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  • Articles  (35)
  • Parathyroid hormone  (35)
  • Springer  (35)
  • 1980-1984  (35)
  • Physics  (35)
  • Energy, Environment Protection, Nuclear Power Engineering
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  • Articles  (35)
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  • Springer  (35)
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  • Physics  (35)
  • Energy, Environment Protection, Nuclear Power Engineering
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  • 1
    Electronic Resource
    Electronic Resource
    Radioimmunoassays for the 28–48 region of parathyroid hormone detect intact hormone but not hormone fragments (1981)
    Springer
    Calcified tissue international 33 (1981), S. 375-380 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Radioimmunoassay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Metabolism of parathyroid hormone (PTH) is known to involve cleavage in the 28-48 region. With the goal of establishing a radioimmunoassay specific for the intact PTH molecule, we have tested the hypothesis that assays specific for the 28-48 region might fail to recognize the hormone fragments arising in vivo. Antisera against native bovine PTH (bPTH) contain antibody species directed at the 28-48 region of bPTH, since (a) 5 of 6 such antisera showed inhibition of binding of125I-labeled bPTH-(1-84) by unlabeled synthetic bPTH-(28-48), and (b) 9 of 9 such antisera bound125I-labeled bPTH-(28-48). The latter radioligand yields assays specific for the 28-48 region; 5 of 5 such assays recognized intact bPTH-(1-84), but none recognized bPTH-(1-34), bPTH-(37-84), or both fragments together. Binding of125I-bPTH-(28-48) to anti-bPTH sera was not inhibited by intact human PTH (hPTH). Likewise, only 1 of 6 antisera against native hPTH would bind125I-bPTH-(28-48) or show inhibition of125I-bPTH-(1-84) binding by unlabeled bPTH-(28-48). This poor immunological cross-reactivity between the 28-48 regions of bPTH and hPTH implies a major conformational transition between the two hormones in the 40–47 region of the molecule where the primary structure differs at 5 of 8 positions. A 28-48 specific assay employing an antiserum raised against both bPTH and hPTH did recognize both bPTH-(1-84) and hPTH-(1-84), but not bPTH-(1-34), hPTH-(1-34), bPTH-(37-84), or hPTH-(44-68). Thus, 6 different 28-48 region-specific assays have been shown to recognize intact PTH but not hormone fragments resembling those thought to be formed in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02409459
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  • 2
    Electronic Resource
    Electronic Resource
    Calcium-mediated enhancement of the cyclic AMP response in cultured bone cells (1981)
    Springer
    Calcified tissue international 33 (1981), S. 409-416 
    Details
    ISSN: 1432-0827
    Keywords: Bone Cells ; Cyclic AMP ; Calcium ; Parathyroid hormone ; Prostaglandin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We have examined the influence of extracellular Ca2+ on cyclic AMP metabolism in an osteoblast-enriched population of bone cells isolated from the calvaria of rat fetuses. The cyclic AMP1 response to stimulators of cyclic AMP formation (PTH and PGE2), but not basal cyclic AMP levels, increased progressively as the extracellular Ca2+ concentration was raised from 0.2 to 4.0 mM. The response to changes in extracellular Ca2+ were rapid (within 3.5 min), and the level of responsivity that characterized each Ca2+ concentration persisted for at least 6 h when the Ca2+ concentration was kept constant. The effect of Ca2+ spanned the entire time course of PTH action, was not accompanied by altered excretion of cyclic AMP from the cells, and was evident at low as well as at high hormone concentrations. Ca2+ augmented the action of PTH in the presence as well as in the absence of cyclic AMP phosphodiesterase inhibitors, and failed to decrease cyclic AMP phosphodiesterase activity in the short term. Mn2+ and, to a smaller degree, Ba2+ substituted for Ca2+ in promoting the cyclic AMP response to PTH. Verapamil, an inhibitor of Ca2+ penetration, blunted the Ca2+-mediated increments in the cyclic AMP response, and the divalent cation ionophore A23187 enhanced these increments. These results indicate that Ca2+ and other cations are positive effectors of the stimulated cyclic AMP response in isolated bone cells. Accumulation into an as yet unknown cellular compartment may be required for the cation effect. The data are most consistent with enhancement of adenylate cyclase reactivity as the mode of cation action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02409464
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  • 3
    Electronic Resource
    Electronic Resource
    In vitro effects of vitamin D3 metabolites on rat calvaria cAMP content (1980)
    Springer
    Calcified tissue international 30 (1980), S. 209-216 
    Details
    ISSN: 1432-0827
    Keywords: Calvarium ; cAMP ; Vitamin D3 metabolites ; Calcium ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Results from in vitro works suggest that 1,25- and 24,25-dihydroxyvitamin D3 (1,25-(OH)2D3 and 24,25-(OH)2D3) act on bone via different mechanisms. The present investigation was performed to study the effect of these two metabolites and of their precursor 25-hyxdroxyvitamin D3 (25-(OH)D3) on bone cAMP content in vitro. Rats' paired half calvaria were incubated under sterile conditions with one vitamin D3 derivative (10−13 to 10−9 M) or with ethanol (0.005 ml for 15 min to 24 h in 1 ml medium containing 0, 0.2, 1, 2, or 3 mM calcium. In some experiments: (a) cycloheximide (10−5M) was added simultaneously with the vitamin D3 metabolites; (b) 1–84 bPTH (5 × 10−8 M) was added for 5 or 15 min at the end of the 24 h incubation. Calvaria were immersed in 1 ml TCA 5% 4°C and homogenized. The cAMP was extracted with diethylether and measured by a competitive protein binding assay. Results bring further evidence for a particular effect of low doses of 24,25-(OH)2D3 (10−9 to 10−12M) and of 25-(OH)D3 (10−9 to 10−11M) on bone, different from that of 1,25-(OH)2D3: cAMP content was higher in 24,25-(OH)2D3- or 25-(OH)D3-treated and lower in 1,25-(OH)2D3-treated calvaria than in ethanol-treated ones with 1 mM calcium. The 1,25-(OH)2D3 effect persisted in calcium-free medium whereas 25-(OH)D3 and 24,25-(OH)2D3 effects could not be observed with 0 mM nor with 3 mM calcium. The required duration of the preincubation (over 1 h) as well as the inhibitory action of cycloheximide may suggest an involvement of protein synthesis in the vitamin D3 metabolites effects. Neither 1,25-(OH)2D3 nor 24,25-(OH)2D3 affected the PTH-induced increase in bone cAMP content.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02408630
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  • 4
    Electronic Resource
    Electronic Resource
    Comparison of fetal rat limb bones and neonatal mouse calvaria: Effects of parathyroid hormone and 1,25-dihydroxyvitamin D3 (1983)
    Springer
    Calcified tissue international 35 (1983), S. 172-176 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; 1,25-Dihydroxyvitamin D3 ; Bone culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The relative responses of fetal rat limb bones and neonatal mouse calvaria to parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) were examined in organ culture. Limb bones were cultured in dishes in BGJ+1 mg/ml bovine serum albumin (bSA) or DMEM+15% heat-inactivated horse serum (hS). Calvaria were either cultured in dishes with one of the above two media or in roller tubes in DMEM+hS. The order of sensitivity to PTH was: calvaria in roller tubes〉limb bones in dishes in DMEM+hS〉limb bones in dishes in BGJ+bSA ≥ calvaria in dishes in DMEM+hS〉calvaria in dishes in BGJ+bSA. The most sensitive system (i.e., calvaria in roller tubes) showed significant resorption in response to 10−10M PTH at 48 h. The least sensitive system did not respond to 3×10−8M PTH after the same length of time. The greater response in DMEM+hS compared with BGJ+bSA appeared to be due to the protein component of the medium. The order of sensitivity to 1,25(OH)2D3 was: calvaria in roller tubes=long bones in culture dishes in BGJ+bSA〉long bones in culture dishes in DMEM+hS〉calvaria in dishes in DMEM+hS〉calvaria in dishes in BGJ+bSA. The most sensitive systems showed resorption in response to 10−11M 1,25(OH)2D3 by 72 h. The least sensitive system failed to respond to 10−9M 1,25(OH)2D3 after the same length of time. The nature of the protein constituent did not seem to influence the response of the limb bones to 1,25(OH)2D3. The results indicated that although the responses of the two bone systems to the calcemic hormones were qualitatively similar, media and culture conditions could markedly affect the sensitivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405027
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of magnesium ion on parathyroid hormone secretion in vitro (1980)
    Springer
    Calcified tissue international 32 (1980), S. 201-206 
    Details
    ISSN: 1432-0827
    Keywords: Magnesium ; Parathyroid hormone ; Secretion ; In vitro ; Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary In a well-defined in vitro perifusion system, the effects of extracellular magnesium concentration (Mg) on parathyroid hormone (PTH) secretion by bovine parathyroid tissue were examined. At Mg less than 0.8 mM, the ability of the glands to secrete hormone maximally in response to low calcium (Ca) stimulation was progressively impaired. Low Mg also impaired the ability of isoproterenol, dibutyryl cyclic AMP and theophylline to stimulate hormone release. The defect in hormone release at low Mg observed in vitro was analogous to the well-documented inhibition of secretion observed in vivo. Increases in Mg from 0 to 0.8 mM rapidly repaired the defect in hormone secretion. At Mg above 1.0 mM there was a Ca-like effect on hormone release, with a progressive decrease in secretion at increased Mg. Although its mechanism is not yet clear, the low Mg effect appears to impair principally the process of hormone release rather than its biosynthesis or storage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02408542
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  • 6
    Electronic Resource
    Electronic Resource
    Influence of calcium depletion on medullary bone of laying hens (1980)
    Springer
    Calcified tissue international 32 (1980), S. 221-228 
    Details
    ISSN: 1432-0827
    Keywords: Medullary bone ; Calcification ; Low-calcium diet ; Parathyroid hormone ; Estrogens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Medullary bone of birds maintained on a low-calcium diet represents a good model to study modifications of matrix composition in calcified tissue undergoing intense formation and resorption. The composition of the bone matrix during the low-calcium diet has been analyzed by both chemical and histological techniques. Sixty White Leghorn pullets 1 year old were used for the experiment. Fifteen birds served as controls and were killed on day zero; the remaining birds were placed on a calcium-deficient diet (0.13% calcium) and sacrificed after 4, 7, and 12 days of treatment in groups of 15. Serum levels of calcium, PTH, and estrogens were also measured. Chemical analysis of the samples were made for total nitrogen, hydroxyproline, hexosamine, hexoses, calcium, and phosphorus. Collagen and proteoglycans of the matrix of medullary bone of the egg-laying hens were found to be affected by the low-calcium diet. They either increased or decreased during the experiment but never in parallel. The increment of serum PTH is considered responsible for the variations in the amount of collagen. The effects of this hormone are magnified by the fall of serum estrogens as shown also by variations in the amounts of noncollagenous protein. In the late phase of the diet the matrix is represented by poorly calcified osteoid tissue rich in noncollagenous protein, i.e., proteoglycans and glycoproteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02408545
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  • 7
    Electronic Resource
    Electronic Resource
    Parathyroid hormone concentration gradients across the human bone marrow (1983)
    Springer
    Calcified tissue international 35 (1983), S. 591-595 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Bone marrow blood ; Antecubital vein blood ; Arterio-venous differences
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Parathyroid hormone (PTH) concentrations were compared in blood drawn from the bone marrow and antecubital vein of patients undergoing marrow biopsy for suspected hematological neoplasia. Radioimmunological analysis revealed that the bone marrow blood had a higher PTH content than blood from the peripheral circulation. Thyroid hormone-binding globulin was not distributed asymmetrically, showing that the gradient is PTH specific. The intact PTH content of marrow blood was 65% greater than that in the venous system, whereas carboxyl regional PTH levels showed a 34% gradient in favor of the marrow. Although the majority of patients were found to have hematological malignancies, there was no discernable influence of tumor on the PTH gradients. The physiological implications and possible origins of the asymmetrical PTH distribution are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405099
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  • 8
    Electronic Resource
    Electronic Resource
    Inhibition by 1,25 dihydroxycholecalciferol of hormonal secretion of rat parathyroid gland in organ culture (1984)
    Springer
    Calcified tissue international 36 (1984), S. 384-391 
    Details
    ISSN: 1432-0827
    Keywords: 1,25(OH)2D3 ; Vitamin D metabolities ; Parathyroid hormone ; PTH secretion regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of vitamin D metabolites on parathyroid hormone secretion was studied using rat parathyroid gland cultured in basal medium Eagle containing 5% serum obtained from thyroparathyroidectomized rat, 1 mM magnesium, and calcium concentration varying from 0.75–2.25 mM, and radioimmunoassay for rat parathyroid hormone (rPTH). 1,25 dihydroxycholecalciferol (1,25(OH)2D3), 5×10−10−2.5×10−8M, consistently decreased rPTH secretion in dose-related manner; the effect reached steady state after 24 hin vitro addition of 1,25(OH)2D3 and was also observed at different medium calcium concentrations (0.75, 1.25, 1.75 mM). Comparison of dose-responses for inhibitory activity of some vitamin D metabolites on rPTH secretion showed: 1,25(OH)2D3=1,24,25(OH)3D3〉1α OHD3〉25 OHD3. Cholecalciferol (10−5M), 24,25-dihydroxycholecalciferol (10−8−10−6M) and 25,26-dihydroxycholecalciferol (5×10−9−5×10−7M) did not inhibit rPTH secretion. Analysis of structural activity relation of vitamin D metabolites studied indicated that 1α or pseudo-1α hydroxylated metabolites or analogs were active in inhibiting rPTH secretion, while, non-1α hydroxylated metabolites were without or were weakly inhibitory only at very high concentrations. This study provides further evidence for a direct role of 1,25(OH)2D3 on a negative feedback loop for regulation of parathyroid gland function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405350
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  • 9
    Electronic Resource
    Electronic Resource
    Use of osmotic minipumps for delivery of parathyroid hormone (1982)
    Springer
    Calcified tissue international 34 (1982), S. 270-272 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Minipumps ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary To determine if osmotic minipumps can be used for the local delivery of parathyroid hormone (PTH), we examined the bone resorbing activity of PTH in minipumps, either removed and assayed in bone organ cultures or released over rat calvaria. Biological activity of PTH was maintained for up to 6 days when the hormone solution contained serum and the minipumps and tubing were siliconized and flushed with diluent prior to use. Addition of cysteine did not enhance activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02411249
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  • 10
    Electronic Resource
    Electronic Resource
    Serum calcitonin concentrations in premature infants during the first 12 weeks of life (1982)
    Springer
    Calcified tissue international 34 (1982), S. 470-473 
    Details
    ISSN: 1432-0827
    Keywords: Calcitonin ; Premature ; Osteopenia ; Hypocalcemia ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Twenty-eight premature infants of mean gestation 30.9±2.5 weeks and mean birth weight 1175±206 g had repeated serum calcitonin concentrations determined over the first 12 weeks of life. Serum calcitonin concentrations slowly fell but remained elevated even at 12 weeks of age [normal adult=71±48, 1 week (N=15)=327±167, 3 week (N=23)=270±129, 6 week (N=16)=249±154, 9 week (N=13)=214±108, 12 week (N=12)=174±11]. Throughout this period, serum total calcium was normal or low (8.4±.8–9.3±1.0). Serum phosphorus was normal or low (6.0±1.4–6.5±1.0), and serum magnesium was normal (1.7±0.24–1.8±0.34). The reason for the sustained elevation of serum calcitonin in these very small, sick, premature infants in unclear.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02411287
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  • 11
    Electronic Resource
    Electronic Resource
    Maintenance of normocalcemia by continuous infusion of the synthetic bovine parathyroid hormone (1–34) in parathyroidectomized rats (1982)
    Springer
    Calcified tissue international 34 (1982), S. 553-557 
    Details
    ISSN: 1432-0827
    Keywords: Serum calcium ; Parathyroidectomized rat ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary This work was conducted to estimate the replacement dose of the synthetic bovine parathyroid hormone [PTH(1–34)] that is required for maintenance of serum calcium (Ca) in parathyroidectomized (PTX) rats. Male rats were PTX and used in this study only if serum Ca was reduced to at least 7 mg/dl. We found that a solution of 2% cysteine, 150 mM NaCl, and 1 mM HCl was superior to 20 mM acetic acid for maintenance of biological activity of PTH (1–34) in situ during the period of hormone infusion studied. The PTH dose—calcemic response relationship was investigated using PTH in doses of 0.6, 1, and 3 U/h. The infusion of 1 U PTH per hour raised Ca to the normal level, whereas rats infused with 0.6 U/h were hypocalcemic and 3 U/h resulted in marked hypercalcemia. To extend this observation we carried out an infusion of 1 U PTH per hour for 14 days. We found that this infusion rate of bovine PTH (1–34) provided a relatively stable level of serum calcium with modest fluctuation from normocalcemic to somewhat hypercalcemic levels for the entire 14-day period of PTH infusion. Serum calcitonin was also elevated during the infusion period and then returned to the initial level when PTH treatment was stopped. After the minipumps containing PTH were removed, the serum Ca dropped rapidly to 5 mg/dl, which was significantly lower than the control (vehicle-infused) or initial values of serum Ca (7 mg/dl). Infusion of PTH at 3 U/h for 4 days did not produce this rebound hypocalcemia after the pumps were removed. Serum Ca in those experiments returned to the initial level after hormone treatment was discontinued.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02411303
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  • 12
    Electronic Resource
    Electronic Resource
    Tissue deposition and metabolism of125I-labeled synthetic amino-terminal parathyroid hormone bPTH(1–34) (1980)
    Springer
    Calcified tissue international 30 (1980), S. 147-150 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Distribution ; Metabolism ; Heterogeneity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The tissue deposition and metabolism of125I-labeled synthetic amino-terminal parathyroid hormone, bPTH(1–34), were studied in rats. In comparison with the intact hormone molecule bPTH(1–84), the synthetic fragment was (a) cleared more rapidly from serum; (b) degraded more rapidly in peripheral tissues; (c) deposited to a greater extent in kidney; (d) deposited to a much smaller extent in liver. In bone, the accumulation of total radioactivity was approximately the same with both labeled hormones. The possible physiological significance of these patterns of distribution and metabolism is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02408619
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  • 13
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    Parathyroid hormone stimulates dentin and bone apposition in the thyroparathyroidectomized rat in a dose-dependent fashion (1983)
    Springer
    Calcified tissue international 35 (1983), S. 586-590 
    Details
    ISSN: 1432-0827
    Keywords: Dentin ; Bone ; Apposition rate ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The dose-dependency of the effects of parathyroid hormone (PTH) on bone and dentin apposition after both intermittent and continuous administration of the hormone was investigated. The purpose was to compare the sensitivity of these two mineralizing tissues to parathyroid hormone and to provide additional information regarding the direct effect of PTH on mineralized tissue formation. Adult rats were thyroparathyroidectomized and 5 groups of 4 or 5 rats each were given daily subcutaneous injections with different doses of bovine parathyroid hormone. Five more groups of 4 rats each were administered equivalent dosages by means of a continuous infusion pump implanted subcutaneously. An additional group of 4 rats served as controls. All animals were labeled with tetracycline injected on days 7, 9, and 11. The animals were killed on day 12 and blood samples were collected for serum calcium determination. The lower metaphysis of the femur and the left and right mandibles were dissected out, and undecalcified sections of plastic-embedded tissues were prepared. The distances between the three tetracycline bands were measured to determine the amount of bone or dentin formation. Results indicated that both dentin and bone apposition increased with higher dosages of hormone. No overall effect of the method of administration was evident. For both methods, bone apposition showed a more pronounced increase over the control levels than dentin apposition. This suggests that, although both osteoblasts and odontoblasts appear to respond directly to PTH, differences do exist in the magnitude and dose-dependency of the response. No causal relationship was found between increases in serum calcium levels and either bone or dentin apposition at the lower dose levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405098
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  • 14
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    Divergent effects of forskolin on 3′,5′ cyclic adenosine monophosphate production and parathyroid hormone secretion (1984)
    Springer
    Calcified tissue international 36 (1984), S. 87-94 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Adenylate cyclase ; 3′5′ cyclic adenosine monophosphate ; Forskolin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Forskolin, a diterpene which directly stimulates adenylate cyclase, markedly stimulated cAMP production in intact rat parathyroid glands and dispersed cells from hyperplastic and adenomatous human parathyroid tissues. Stimulation of cAMP production in human parathyroid adenomas occurred as early as 2 min and continued for at least 2 h; furthermore, a dose-response relationship was observed, with a maximal 80-fold cAMP response occurring at 100 µM forskolin. When PTH secretion by rat or human parathyroid tissues was studied at low (0.5 mM) and high (2.5 mM) extracellular Ca2+ in either the presence or absence of forskolin, no significant stimulation by forskolin was observed at 15 min, 1 h, and 2 h. When 10 human parathyroid specimens were studied with varying concentrations of forskolin at 1 mM Ca2+, 6 failed to show stimulation of PTH secretion and 4 showed modest but detectable increases in PTH that did not appear dose-related. We conclude that (1) at low and high Ca2+ levels, marked stimulation of cAMP production by forskolin can occur without a corresponding increase in PTH secretion; (2) inhibition of PTH secretion by high extracellular Ca2+ levels continues unchanged despite stimulation of cAMP production by forskolin; and (3) at intermediate Ca2+ levels (1.0 mM), PTH secretion is affected either minimally or not at all by forskolin in human hyperparathyroid tissue preparations. The marked stimulation of parathyroid adenylate cyclase by forskolin without concomitant increases in PTH secretion in the majority of tissues suggests that the level of cAMP production is not a primary or sufficient determinant of hormone secretion.
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    URL: http://dx.doi.org/10.1007/BF02405299
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  • 15
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    Protamine: A powerfulin vivo inhibitor of bone resorption (1984)
    Springer
    Calcified tissue international 36 (1984), S. 189-193 
    Details
    ISSN: 1432-0827
    Keywords: Protamine ; Hypocalcemia ; Parathyroid hormone ; Bone resorption ; Bone turnover
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Protamine is shown to be a powerful disrupter of calcium homeostasis, acutely inducing a severe hypocalcemia in both rabbits and rats. The magnitude of its effect correlates with bone turnover. Protamine does not significantly alter the renal excretion of calcium, and is effective whether or not there is calcium present in the gut. Protamine causes a significant fall in the specific activity of45Ca in the blood in animals whose bone has been prelabeled with45Ca. These data suggest that protamine induces hypocalcemia by blocking calcium efflux from bone. Further work seems indicated to define the biochemical mechanism of this action.
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    URL: http://dx.doi.org/10.1007/BF02405316
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  • 16
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    Adriamycin inhibits PTH-mediated but not PGE2-mediated stimulation of cyclic AMP formation in isolated bone cells (1984)
    Springer
    Calcified tissue international 36 (1984), S. 279-284 
    Details
    ISSN: 1432-0827
    Keywords: Bone cells ; Parathyroid hormone ; PGE2 ; Adriamycin ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We have examined the effect of adriamycin, an anthracycline antibiotic which modifies plasma membrane functions, on the cyclic AMP response to PTH and PGE2 in isolated osteoblastlike cells. Adriamycin blunted the increment in bone cell cyclic AMP caused by exposure to PTH. This effect appeared rapidly (within 3 min after bone cells were exposed to adriamycin) and disappeared soon after exposure of adriamycin-treated cells to adriamycin-free incubation medium. Inhibition was evident over the entire time course of PTH action, at low as well as high PTH concentrations, and was one-half maximal at 31 µM adriamycin. It could not be attributed to alterations in cyclic AMP exodus, degradation or interference with the cyclic AMP assay, nor to impaired cell viability. Adriamycin also reduced the stimulatory effect of PTH on adenylate cyclase activity in a crude plasma membrane preparation. By contrast, adriamycin failed to modify the effects of PGE2 on cyclic AMP generation in intact bone cells, and on adenylate cyclase activity in broken cells. Moreover, concentrations of adriamycin that blunted the effect of PTH on adenylate cyclase activity did not inhibit the stimulatory effects of sodium fluoride or of GppNHp. These results suggest that adriamycin selectively alters the interaction between PTH and its receptor or impairs the transmission of information from hormone-receptor complex to adenylate cyclase (or both), perhaps by binding to specific lipid domains in the plasma membrane. Structural analogues of adriamycin, which vary in their lipophilic properties, also varied in their capacity to perturb the cyclic AMP response. One such analogue in fact inhibited the response to PGE2, and several appeared to augment the PGE2 effect. These substances may well be useful in probing the membrane properties required for selectivity in hormone action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405331
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  • 17
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    Effects of vitamin D and parathyroid hormone on cyclic AMP production by bone cells isolated from rat calvariae (1984)
    Springer
    Calcified tissue international 36 (1984), S. 320-326 
    Details
    ISSN: 1432-0827
    Keywords: Calcium ; Vitamin D deficiency ; 1,25(OH)2D3 ; Parathyroidectomy ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Studies presented here were designed to investigate further the basis for an impaired cAMP response to parathyroid hormone (PTH) in osteoblastlike calvarial bone cells isolated from vitamin D-deficient rat pups. The goal was to perturb Ca, PTH, and vitamin Din vivo in order to see which factors might be responsible for the impairedin vitro bone cell cAMP response. Pups either were parathyroidectomized (PTX) 3–5 days, implanted with osmotic minipumps delivering high doses of PTH, given repeated, high doses of 1,25(OH)2D3, or were D-deficient (-D, i.e., born and suckled by D-deficient mothers). Osteoblastlike bone cells, isolated by sequential enzyme digestion and centrifugation, were exposed to PTH for 5 min in the presence of a phosphodiesterase inhibitor. In bone cells isolated from -D rat pups, both basal and PTH-induced cAMP accumulation were significantly lower than in +D bone cells. Earlier, we had shown that two daily injections of -D pups with 50 ng 1,25(OH)2D3 restores this reduced bone cAMP response of -D pups toward normal. In the present study, neither basal nor PTH-induced bone cell cAMP accumulation was affected by subjecting D-replete pups to PTX, PTH infusion, or repeated high doses of 1,25(OH)2D3 despite the fact that each treatment markedly changed serum Ca or serum immunoreactive PTH. The results indicate that the impaired bone cell cAMP response seen in -D pups is not a direct result of chronic hypocalcemia and that the “heterologous desensitization” seenin vitro with added 1,25(OH)2D3 could not be duplicated byin vivo treatment of +D pups with supraphysiologic doses of 1,25(OH)2D3. Finally the lack of alteration in the bone cell cAMP response to PTHin vitro after chronic PTH infusionin vivo fails to support the notion that the impaired response in -D bone cells can be explained entirely by “homologous desensitization” induced by high circulating levels of PTH in the hypocalcemic, -D rat pup.
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    URL: http://dx.doi.org/10.1007/BF02405337
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    Influence of pregnancy on immunoreactive parathyroid hormone levels (1982)
    Springer
    Calcified tissue international 34 (1982), S. 9-12 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Pregnancy ; Nephrogenous cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Parathyroid hormone (PTH) metabolism in pregnancy has not been clearly defined. Studies have reported either increased or unchanged values of immunoreactive PTH (iPTH). However, iPTH levels do not necessarily correlate with hormonal bioactivity due to the presence of immunoreactive but nonbioactive PTH fragments. In this study we evaluated PTH metabolism in the third trimester of pregnancy by determining iPTH blood levels as well as the biological effects of PTH, assessed by tubular maximum phosphate reabsorption (TmP) and nephrogenous cAMP (ncAMP) excretion, in 10 young, healthy pregnant patients (mean gestational age 35 weeks) and 10 young, healthy age-matched female controls. Pregnancy was associated with a significant increase in creatinine clearance (146±13 vs 106±9 ml/min,P〈0.01), and a significant decrease in total fasting serum calcium (8.4±0.1 vs 9.0±0.1 mg/dl,P〈0.001) and serum albumin (3.6±0.1 vs 4.2±0.1 g/dl,P〈0.001). There was no significant difference in iPTH (3.7±0.4 vs 4.3±0.5 µlEq/ml), serum phosphorus (3.6±0.1 vs 3.8±0.2 mg/dl), TmP (3.61±0.13 vs 3.75±0.25 mg/100 ml GFR), or ncAMP (1.68±0.20 vs 1.88±0.23 nmoles/100 ml GFR) between the two groups. Pregnancy was attended by a significant increase in fasting urinary calcium to creatinine ratio (0.14±0.03 vs 0.06±0.01,P〈0.05), an index of bone resorption. The data suggest that the biological effects of PTH are unchanged in pregnancy, and that reported increments in 1,25(OH)2 vitamin D in pregnancy are not regulated by changes in either PTH, calcium, or phosphate.
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    URL: http://dx.doi.org/10.1007/BF02411200
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  • 19
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    Comparison of parathyroid hormone and calcium ionophore A23187 effects on bone resorption and nucleic acid synthesis in cultured fetal rat bone (1982)
    Springer
    Calcified tissue international 34 (1982), S. 495-500 
    Details
    ISSN: 1432-0827
    Keywords: Calcium ionophore A23187 ; Parathyroid hormone ; 45Ca release ; DNA concentration ; Nucleic acid synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary It has recently been demonstrated that calcium ionophore A23187 mimics certain of the effects of parathyroid hormone (PTH) on bone in vitro, including stimulation of45Ca release and cAMP formation. To further examine the relative effects of these two agents on bone cell metabolism, we compared the effects of synthetic PTH 1–34 (50 ng/ml) and calcium ionophore A23187 (0.5µg/ml) on45Ca release, DNA concentration, and nucleic acid synthesis in fetal rat forelimb rudiments cultured for periods up to 120 h. Both agents stimulated45Ca release; however, the effects of PTH were apparent after a shorter period of exposure. Bone DNA concentration (expressed asµg DNA/mg bone) was not affected by PTH but was significantly increased relative to control values by exposure to A23187 for 8–120 h of incubation. PTH increased the incorporation of3H-thymidine into DNA at 30 and 48 h, and increased the incorporation of14C-uridine into RNA at 48 h, time points which corresponded to a period of accelerated PTH stimulation of45Ca release. In contrast,3H-thymidine and14C-uridine incorporation were both uniformly suppressed by A23187 at all time points examined. Thus the increased DNA concentration observed in A23187-treated rudiments appeared to be the result of a decreased rate of bone maturation and mineralization. The markedly different patterns of nucleic acid synthesis in response to PTH and A23187 suggest that these agents differ significantly in their mechanisms of action on bone cell metabolism.
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    URL: http://dx.doi.org/10.1007/BF02411291
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  • 20
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    Calcitonin and parathyroid hormone in newborn infants with fracture of the clavicle (1984)
    Springer
    Calcified tissue international 36 (1984), S. 357-360 
    Details
    ISSN: 1432-0827
    Keywords: Calcitonin ; Parathyroid hormone ; Calcium ; Newborn ; Fracture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Determinations of serum calcium (Ca), phosphorus (P), calcitonin (CT), and parathyroid hormone (PTH) were carried out in 36 full-term newborn infants with fracture of the clavicle (CF) and in 46 normal neonates (N). At the 6th hour of life the CF neonates demonstrated lower serum Ca and higher serum CT in comparison with normal infants. In the hours following, no significant differences between the two groups for the Ca levels were found, whereas serum CT remained significantly higher in the CF newborns at the 24th, 48th, and 72nd hour of life. Significant differences between normal and CF infants in the PTH serum levels were detected only at the 48th hour, when PTH was lower in the CF newborns. The results of this investigation indicate that the fracture of the clavicle is a significant and peculiar factor in stimulating CT secretion. Serum Ca level appeared to be controlled by CT rather than auto-regulating the secretion of the hormone.
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    URL: http://dx.doi.org/10.1007/BF02405346
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  • 21
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    Canine lymphosarcoma: A model for study of the hypercalcemia of cancer (1980)
    Springer
    Calcified tissue international 30 (1980), S. 127-133 
    Details
    ISSN: 1432-0827
    Keywords: Lymphosarcoma ; Hypercalcemia ; Parathyroid hormone ; Prostaglandins ; bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Lymphosarcoma of domestic dogs is often accompanied by hypercalcemia. We have carried out studies to determine the usefulness of this common canine neoplasm as a model for paraneoplastic hypercalcemia. The study population consisted of 27 healthy control dogs, 13 with hypercalcemic lymphosarcoma, and 28 normocalcemic dogs with lymphosarcoma. Studies included measurement of circulating calcium, phosphorus, creatinine, immunoreactive parathyroid hormone (iPTH) and prostaglandin E2 (iPGE2) concentrations, and determination of in vitro bone-resorbing activity in supernatant culture media from normal and neoplastic lymphoid tissue. Hypercalcemia was severe in the affected group (mean ± SE, 14.9±0.5 mg/dl, normals 10.1±0.1 mg/dl) and associated with decreased renal function (serum creatinine 2.0±0.4 mg/dl, normal 0.8±0.1 mg/dl,P〈0.001). Radiographs and autopsies showed no bone destruction. Despite renal insufficiency, hypercalcemic dogs had subnormal serum iPTH concentrations (12±1 ngEq/ml, normals 37±6 ngEq/ml,P〈0.05). Creatinine and iPTH were normal in the normocalcemic tumor-bearing dogs. When antitumor therapy lowered serum calcium to normal or below in 5 hypercalcemic dogs, iPTH rose markedly in all while renal function improved. Plasma iPGE2 levels did not differ among the groups, nor did high-dose oral aspirin or indomethacin treatment lower elevated serum calcium (two dogs). Culture media from normal lymphoid tissue and control culture media had no effect on release of45Ca from prelabeled fetal mouse forelimb bones, but media from tumor tissue increased45Ca release. However, correlation of serum calcium with in vitro bone-resorbing activity was poor. We conclude that (a) the hypercalcemia of canine lymphosarcoma is mediated not by bone metastases or “ectopic” secretion of PTH, but by other bone-resorbing factors secreted by the tumors; and (b) canine lymphosarcoma may be a valuable experimental model for study of some human paraneoplastic hypercalcemias.
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    URL: http://dx.doi.org/10.1007/BF02408617
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  • 22
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    In vitro perifusion for the study of parathyroid hormone secretion: Effects of extracellular calcium concentration and beta-adrenergic regulation on bovine parathyroid hormone secretion in vitro (1980)
    Springer
    Calcified tissue international 32 (1980), S. 19-27 
    Details
    ISSN: 1432-0827
    Keywords: Perifusion ; Parathyroid hormone ; In vitro ; Calcium ; Beta regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary An in vitro perifusion system was used to study parathyroid hormone (PTH) secretion in response to calcium (Ca) and beta-adrenergic agents. Perifused parathyroid tissue responded to changes in Ca within the physiologic range during experiments up to 5 h. There was rapid secretory stimulation after exposure to low Ca, with the maximum response being observed at 20 min. Normal bovine glands showed a Ca-independent nonsuppressible component of PTH release at concentrations of Ca above physiologic. 1-isoproterenol produced rapid stimulation of PTH release, the response being blocked by a beta antagonist. The maximum secretory response to either low Ca (0.5 mM) or 1-isoproterenol (10−5 M) was enhanced when the two stimuli were applied simultaneously. The response to isoproterenol was blocked by raising Ca to 2.5 mM. Although d,l-propranolol (10−4 M) caused mild suppression of PTH release at a Ca of 1.25 mM, it did not cause additional suppression at 2.5 mM Ca nor did it decrease the response to 0.5 mM Ca stimulation. The secretory response of the gland to low Ca was sustained at a level more than double the baseline rate. The response to isoproterenol was more transient, with a return to or toward baseline secretion within 60 min. These results suggest that beta agonists and low Ca have separate but related mechanisms for stimulating PTH release and may affect different pools of hormone. The perifusion system described is a relatively simple technique for assessing the kinetics and interactions of various stimulators of PTH secretion.
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    URL: http://dx.doi.org/10.1007/BF02408518
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  • 23
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    Hormonal and nonhormonal desensitization in isolated bone cells (1980)
    Springer
    Calcified tissue international 32 (1980), S. 95-103 
    Details
    ISSN: 1432-0827
    Keywords: Desensitization ; Bone cells ; Parathyroid hormone ; Cyclic AMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Prior exposure to PTH markedly decreased the responsiveness of isolated, cultured bone cells to the stimulatory effect of the hormone on cyclic AMP formation. This process of desensitization developed within 30 min, persisted during prolonged incubation of the cells in PTH-free medium, and could not be attributed to enhanced excretion of cyclic AMP from the cells, nor to the extracellular accumulation of an inhibitor of PTH action. Adenylate cyclase activity in a subcellular fraction derived from PTH-treated cells was refractory to PTH and to sodium fluoride. These results indicate that PTH-mediated desensitization reflects, at least in part, impaired cyclic AMP formation. Adenosine and PGE2, known stimulators of bone cell cyclic AMP formation, elicited agonist-specific desensitization, and also desensitized bone cells to the effects of subsequently added PTH. PTH blunted the cellular response to adenosine, but not to PGE2. Modest refractoriness to PTH was evident in cells that had been treated previously with the cyclic AMP phosphodiesterase inhibitors IBMX, theophylline, and Bt2cAMP, whereas treatment with sodium butyrate had no effect. The actions of the inhibitors, like that of PTH, were rapid in onset and long-lasting. Desensitization caused by previous treatment with the phosphodiesterase inhibitors, and with PTH itself, was accompanied by enhanced phosphodiesterase activity in bone cell homogenates. Induction of phosphodiesterase activity may well contribute to desensitization in the bone cell system.
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    URL: http://dx.doi.org/10.1007/BF02408528
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  • 24
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    Relative sensitivity of kidney and bone to the amino-terminal fragment b-PTH (1–30) of native bovine parathyroid hormone: Implications for assessment of bioactivity of parathyroid hormone fragments in vivo and in vitro (1983)
    Springer
    Calcified tissue international 35 (1983), S. 520-525 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Adenylate cyclase activation ; Amino-terminal fragment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Adenylate cyclase activation in renal cortical membranes is widely used to assess the potency of parathyroid hormone (PTH) and hormonal fragments. Recent studies, however, suggest that the structural requirements for biological activity of PTH in bone may differ from those in kidney. In isolated perfused canine bone, cyclic AMP production is markedly increased by syn-b-PTH (1–34) whereas intact b-PTH (1–84) has minimal effect. Furthermore, a potent inhibitor of PTH stimulated adenylate cyclase activity, Nle8Nle18Tyr34 syn-b-PTH (3–34) NH2, devoid of biological activity in kidney, is an agonist in isolated bone. The present studies examine the effects in bone and kidney of the amino-terminal fragment b-PTH (1–30), prepared by cleavage of intact b-PTH (1–84) by Cathepsin Bin vitro. In basolateral canine renal cortical membranes, b-PTH (1–30) was less active than syn-b-PTH (1–34) in its ability to stimulate adenylate cyclase. Half maximal stimulation of adenylate cyclase activity by b-PTH (1–30) was 50 nM compared with 2 nM for syn-b-PTH (1–34). Maximum enzyme activation by b-PTH (1–30) reached only 50% of the activation by syn-b-PTH (1–34). Addition of Gpp(NH)p (1 mM) increased the affinities for both peptides. The relative difference in potency, however, remained unchanged. In contrast, in isolated bone, b-PTH (1–30) and syn-b-PTH (1–34) were equipotent in increasing cyclic AMP production. These data provide further evidence for differences in the structural requirements for PTH activity in bone and kidney and suggest that bioassays of PTH and PTH fragments in kidney may not accurately reflect the effects of PTH in bone.
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    URL: http://dx.doi.org/10.1007/BF02405087
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  • 25
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    Inhibition of parathyroid hormone-stimulated bone resorption by monovalent cation ionophores (1982)
    Springer
    Calcified tissue international 34 (1982), S. 239-244 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Monovalent ionophores ; bone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The actions of divalent cation ionophores on bone resorption in vitro are complex; both enhancement of resorption and inhibition of stimulated resorption have been observed with the ionophore A23187. We have found in neonatal mouse calvaria, in which divalent ionophores were only inhibitory, that monovalent cation ionophores were even more potent inhibitors of stimulated bone resorption. Nigericin, monensin, and X206 each inhibited the release of calcium (Ca) from calvaria that were stimulated to resorb by 0.1 U/ml parathyroid hormone (PTH). Actions of the three ionophores were dose dependent and were maximal at 10−7M, 3×10−7M, and 1.2×10−7M, respectively, compared to A23187, which was maximally inhibitory at 2×10−6M. After pretreatment with nigericin alone or together with PTH for 24 h, inhibition of stimulated resorption was partially reversible. Prolonged (48 h) treatment, either with ionophore alone or together with PTH, caused irreversible inhibition of stimulated Ca release. However, the ionophore was only partially inhibitory if it was added to calvaria stimulated by pretreatment with PTH alone for 24 or 48 h. Resorption stimulated by prostaglandin E2, 1,25-dihydroxyvitamin D3, and epidermal growth factor was also inhibited by monovalent ionophores, indicating that the inhibition was not at the level of the PTH receptor. In addition, ionophores did not lower basal or PTH-stimulated production of cyclic AMP by calvaria. Submaximal doses of nigericin were synergistic with calcitonin or ouabain in inhibiting PTH-stimulated resorption. These results are consistent with the hypothesis that stimulated release of Ca from bone occurs by a Na/Ca exchange mechanism. Thus monovalent cation ionophores would increase intracellular Na+, thereby decreasing the Na gradient across bone cell membranes, leading to conditions unfavorable for Ca efflux coupled to further Na influx.
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    URL: http://dx.doi.org/10.1007/BF02411244
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  • 26
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    In vitro effects of aluminum on bone phosphatases: A possible interaction with bPTH and vitamin D3 metabolites (1982)
    Springer
    Calcified tissue international 34 (1982), S. 280-284 
    Details
    ISSN: 1432-0827
    Keywords: Calvarium ; Phosphatase ; Aluminum ; Vitamin D3 metabolites ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The present study was undertaken to test the in vitro action of aluminum on bone phosphatase activities and the possible interaction of this metal with parathyroid hormone (bPTH) or vitamin D3 dihydroxymetabolites [1,25- and 24,25(OH)2D3). Three-day-old rat calvaria were incubated for 24 h with one of the following: bPTH at 5×10−8M, 1,25-or 24,25(OH)2D3 at 2.5×10−9M, Al at concentrations ranging from 3×10−11M to 6×10−6M, or their corresponding solvents. Al effects were also investigated when the medium phosphate or calcium concentrations were modified. In some experiments, Al was added simultaneously with bPTH or one of the vitamin D3 metabolites at the beginning of the 24 h incubation. At the end of all incubations, acid and alkaline phosphatase activities were measured in bone cytoplasmic extract. The results show that: (a) When compared to the value found in half calvaria incubated in a control medium, the bone acid and alkaline phosphatase content is significantly higher in paired halves incubated with Al (3×10−11M to 1.5×10−6M) as well as with bPTH, 1,25-, or 24,25(OH)2D3 and sharply decreased with higher Al concentrations (6×10−6M). (b) The Al effect on phosphatase activities is modified in a free phosphate or a free calcium medium. (c) The presence of Al at 1.5×10−6M or 6×10−6M significantly decreases the bPTH or 1,25(OH)2D3-induced stimulation of bone phosphatase activities. (d) A similar interaction could not be found between Al and 24,25-(OH)2D3.
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    URL: http://dx.doi.org/10.1007/BF02411251
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  • 27
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    Role of parathyroid hormone and 1,25-dihydroxyvitamin D3 in the development of osteopenia in oophorectomized rats (1982)
    Springer
    Calcified tissue international 34 (1982), S. 510-514 
    Details
    ISSN: 1432-0827
    Keywords: Rats ; Osteopenia of oophorectomy ; 1,25-Dihydroxyvitamin D3 ; Parathyroid hormone ; Osteoporosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of ovarian insufficiency on calcium metabolism has been thought to involve an increased bone resorptive effect of parathyroid hormone and possible impaired synthesis of 1,25-dihydroxyvitamin D3. In the present study a rat model allowing for controlled serum levels of parathyroid hormone and 1,25-dihydroxyvitamin D3 was used. Oophorectomy in this species is associated with increased serum levels of 1,25-dihydroxyvitamin D3 and decreased bone mass. Although thyroparathyroidectomy increased bone mass, an increased sensitivity of bone to parathyroid hormone in oophorectomized rats was not observed. Thus the development of the osteopenia did not seem to be related to increased parathyroid hormone sensitivity or to reduced levels of 1,25-dihydroxyvitamin D3. Exogenous 1,25-dihydroxyvitamin D3 increased bone mass in oophorectomized as well as intact rats. Intestinal calcium transport was increased by moderate doses of 1,25-dihydroxyvitamin D3. Intestinal calcium transport was also reduced by thyroparathyroidectomy and increased by the administration of parathyroid extract. A tendency for increased accumulation of 1,25-dihydroxyvitamin D3 in blood in oophorectomized rats has been noted. It is suggested that the tendency to hypercalcemia in ovarian-insufficient females given 1-hydroxylated vitamin D compounds may be related to a diminished metabolism of 1,25-dihydroxyvitamin D3.
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    URL: http://dx.doi.org/10.1007/BF02411294
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  • 28
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    Development of the cyclic AMP response to parathyroid hormone and prostaglandin E2 in the embryonic chick limb (1981)
    Springer
    Calcified tissue international 33 (1981), S. 641-648 
    Details
    ISSN: 1432-0827
    Keywords: Cyclic AMP ; Parathyroid hormone ; Prostaglandin E2 ; Chondrogenesis ; Chick limb cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The developing chick limb was studied to determine the ability of parathyroid hormone (PTH) and prostaglandin E2 (PGE2) to increase intracellular cyclic AMP (cAMP) during various stages of development. All developmental stages examined (stages 20–21, 24–25, and 26–28) responded to PGE2 when the cells were assayed immediately following the removal of the limbs from the embryos. In contrast, only stage 26–28 limb cells responded to PTH when assayed in a similar manner. The response to PTH was temporally correlated with the appearance of cartilage matrix in vivo. Undifferentiated limb cells were also cultured and assayed at various times for hormone responsiveness. Stage 24–25 high-density cell cultures responded initially to PGE2 but not to PTH. However, by 36 h and in all subsequent itme intervals tested, the response to PTH was significantly greater than that to PGE2. The PTH receptor, in contrast to that of PGE2, was shown to be sensitive to trypsin treatment, but could be regenerated during subsequent cell culture. The majority of the hormoneresponsive cells were found in cartilaginous regions of the limb, and were shown to respond to both hormones in a dose-dependent manner. The PTH-induced cAMP response was affected by low cell density and mouse serum, both of which significantly inhibit the chondrogenic potential of cultured limb cells. These findings are consistent with a temporal correlation between the development of the PTH response and chondrogenesis in vivo.
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    URL: http://dx.doi.org/10.1007/BF02409502
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  • 29
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    Analogues of an in vitro parathyroid hormone inhibitor: Modifications at the amino terminus (1981)
    Springer
    Calcified tissue international 33 (1981), S. 153-157 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Inhibitors ; Analogues ; Receptor binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Four analogues of parathyroid hormone were synthesized, based on a sequence previously shown to yield an in vitro inhibitor of PTH action. Binding properties of the analogues to presumed parathyroid hormone receptors were evaluated. Each of these analogues contains a structural alteration of the amino terminus of the compound [Nle-8,Nle-18,Tyr-34]bPTH-(3-34)amide. Each of the analogues—[desamino-Ser-3, Nle-8, Nle-18, Tyr-34]bPTH-(3-34)amide, [acetyl-Glu-4,Nle-8,Nle-18,Tyr-34]bPTH-(3-34)amide, [d-Ser-3,Nle-8,Nle-18,Tyr-34]bPTH-(3-34)amide, and [pyroGlu-4,Nle-8,Nle-18,Tyr-34]bPTH-(3-34)amide—contains modifications selected to diminish or eliminate the weak PTH-like agonist properties detected in the parent compound in vivo. To permit valid comparison of receptor-binding properties, all the analogues were derived from a common solid-phase synthesis. When assayed in the renal adenylate cyclase assay, each of the compounds inhibited completely PTH-stimulated adenylate cyclase activity and was devoid of PTH-like agonist activity. To compare the binding affinity of the analogues for parathyroid hormone binding sites, the peptides were evaluated in a parathyroid hormone renal radioreceptor assay. Each peptide demonstrated a binding affinity comparable with one another and only slightly weaker than that of the unmodified inhibitory analogue, [Nle-8,Nle-18,Tyr-34]bPTH-(3-34)amide. These studies demonstrate that it is possible to alter the amino terminus of parathyroid hormone analogues without causing a dramatic decline in affinity for the parathyroid hormone receptor. Preservation of high receptor-binding affinity in these analogues indicates that synthesis of one or several of these peptides on a scale sufficiently large to permit in vivo evaluation of both agonist and antagonist properties is warranted.
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    URL: http://dx.doi.org/10.1007/BF02409428
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    Alkaline phosphatase inhibition by parathyroid hormone and isoproterenol in a clonal rat osteosarcoma cell line. Possible mediation by cyclic AMP (1982)
    Springer
    Calcified tissue international 34 (1982), S. 59-66 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Alkaline phosphatase ; Cyclic AMP ; Osteosarcoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of parathyroid hormone (PTH 1–34 bovine) on alkaline phosphatase activity was investigated in an osteoblast-like clonal cell line derived from rat osteosarcoma (ROS 17/2). ROS 17/2 alkaline phosphatase resembled the bone enzyme in levamisole sensitivity and electrophoretic mobility but differed in heat stability. The specific activity of ROS 17/2 alkaline phosphatase increased with time in culture. This increase was inhibited by PTH (1–34) and (-)-isoproterenol in a dose-dependent manner starting at near-physiological hormone concentrations. The ID50 values were 0.02 nM for PTH (1–34) and 1.7 nM for isoproterenol. The two hormones stimulated ROS 17/2 adenylate cyclase, albeit at higher concentrations: Km values were 13 nM for PTH (1–34) and 16 nM for isoproterenol. The rise in alkaline phosphatase was also inhibited by dibutyryl cyclic AMP and 8-bromocyclic AMP (0.1 mM). These findings further document the osteoblastic properties of the ROS 17/2 osteosarcoma cell line, suggest that PTH inhibition of alkaline phosphatase represents a physiological response to the hormone in these cells, and implicate cyclic AMP as a mediator of this PTH effect.
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    URL: http://dx.doi.org/10.1007/BF02411210
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    Parathyroid hormone and calcitonin interactions in bone: Irradiation-induced inhibition of escape in vitro (1982)
    Springer
    Calcified tissue international 34 (1982), S. 197-203 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Calcitonin ; Bone ; Escape ; Irradiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Calcitonin (CT) inhibits hormonally stimulated bone resorption only transiently in vitro. This phenomenon has been termed “escape,” but the mechanism for the effect is not understood. One possible explanation is that bone cell differentiation and recruitment of specific precursor cells, in response to stimulators of resorption, lead to the appearance of osteoclasts that are unresponsive to CT. To test this hypothesis, cell proliferation in neonatal mouse calvaria in organ culture was inhibited by irradiation from a cobalt-60 source. At a dose of 6000 R, [3H]thymidine incorporation into intact calvaria was inhibited approximately 90%. Irradiation had no effect on the resorptive response to 0.1 U/ml parathyroid hormone (PTH). However, irradiation induced a dose-dependent inhibition of the escape response which was maximal at 6000 R. A dose of 6000 R did not affect the binding of125I-salmon CT to calvaria and decreased PTH stimulation of cyclic AMP release from bone without affecting the cyclic AMP response to CT. Although irradiation caused a dose-dependent inhibition of DNA synthesis, the dose-response curves for that effect and inhibition of escape were not superimposable. A morphologic study of hormonally treated calvaria demonstrated that irradiation prevented the early increase in number of osteoclasts in PTH-treated calvaria that had been observed previously in unirradiated bones. Autoradiography showed that irradiation also prevented the PTH-stimulated recruitment of newly divided mononuclear cell precursors into osteoclasts. This may be correlated with the effect of irradiation to prevent the loss of responsiveness to CT in the presence of PTH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02411233
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  • 32
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    Regulation of calcium absorption by 1,25,dihydroxy-vitamin D—Studies of the effects of a bisphosphonate treatment (1982)
    Springer
    Calcified tissue international 34 (1982), S. 317-320 
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    ISSN: 1432-0827
    Keywords: 1,25-Dihydroxy-vitamin D ; Calcium absorption ; Parathyroid hormone ; Bisphosphonate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary In 10 patients with Paget's disease of bone and 2 patients with osteoporosis, we studied the effects of hypocalcemia and hypophosphatemia induced by disodium-(3-amino-1-hydroxypropylidene)-1,-bisphosphonate (APD) treatment on the serum concentration of PTH and 1,25-dihydroxyvitamin D [1,25(OH)2D3] and on calcium absorption and balance. The fall in serum calcium and phosphate was associated with a rise in the serum concentration of PTH and 1,25(OH)2D3, coupled with increases in net calcium absorption and calcium balance. The concentration of 1,25(OH)2D3 was significantly related (P〈0.001) to the serum calcium (r=0.66), the serum phosphate (r=0.78), and the serum PTH (r=0.71), confirming the interrelated control of these parameters on 1,25(OH)2D3 production. Moreover, the rise in 1,25(OH)2D3 caused an appropriate rise in calcium absorption (r=0.74) and calcium balance (r=0.86), showing that this vitamin D metabolite contributes as a hormone to calcium homeostasis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02411260
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  • 33
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    Electronic Resource
    Abnormal skeletal response to parathyroid hormone in dogs with chronic uremia (1982)
    Springer
    Calcified tissue international 34 (1982), S. 403-407 
    Details
    ISSN: 1432-0827
    Keywords: Cyclic AMP ; Parathyroid hormone ; Bone ; Chronic uremia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The release of cyclic AMP from bone in response to stimulation with PTH 1–34 was examined in 20 dogs with long-term chronic renal failure (CRF) produced by unilateral nephrectomy and contralateral partial renal artery ligation. After 9 to 15 months of uremia, the tibiae were removed and perfused in vitro. Seven dogs with CRF served as controls, 7 dogs with CRF were treated with 24,25(OH)2D3 — 2.5 µg per day, and 6 CRF dogs underwent thyroparathyroidectomy (TPTX) 42 h before they were sacrificed. The release of cyclic AMP from bone in response to PTH 1–34 in the CRF dogs was severely reduced compared to the response observed in 7 dogs with normal renal function (net accumulation of cyclic AMP release 86±8.5 versus 426±59.0 pmol/30 min). Long-term treatment of uremic dogs with 24,25(OH)2D3 had no effect on the release of cyclic AMP by bone. However, the release of cyclic AMP was restored to normal levels in the CRF dogs that underwent thyroparathyroidectomy. All CRF dogs had secondary hyperparathyroidism and the fact that TPTX returned the cyclic AMP response to normal values suggests that desensitization to PTH of the adenylate cyclase system of bone exists in chronic uremia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02411275
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  • 34
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    Electronic Resource
    Effect of aluminum and parathyroid hormone on osteoblasts and bone mineralization in chronic renal failure (1984)
    Springer
    Calcified tissue international 36 (1984), S. 133-138 
    Details
    ISSN: 1432-0827
    Keywords: Aluminum ; Parathyroid hormone ; Bone ; Renal failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Bone aluminum, quantitative bone histology, and plasma parathyroid hormone (PTH) were compared in 29 patients undergoing chronic hemodialysis. Histologic techniques included double tetracycline labeling and histochemical identification of osteoclasts and osteoblasts. Bone aluminum was measured chemically by flameless atomic absorption spectrophotometry, and histochemically. When measured chemically, the bone aluminum was 67±46 (SD) mg/kg dry weight (normal 2.4±1.2 mg/kg); histochemically, aluminum was present at 2.9±4.4% of trabecular surface. The biochemical and histochemical results agreed well (r=0.80,P〈0.001). No double tetracycline labels were seen at the mineralization front where aluminum was deposited, indicating cessation of mineralization at these sites. The osteoblast surface correlated positively with plasma PTH (r=0.67,P〈0.001) and negatively with bone aluminum level (r=−0.42,P〈0.05). Multiple linear regression showed a correlation of aluminum with osteoblasts additional to that of PTH, consistent with a direct effect of aluminum in depressing osteoblast numbers. Though a relationship between PTH and chemically determined bone aluminum level could not be demonstrated, there was a negative correlation between osteoclast count and aluminum, and the nine patients with severe hyperparathyroid bone disease had lower chemically determined aluminum levels than the other patients. These results suggest that aluminum (a) directly inhibits mineralization, (b) is associated with decreased PTH activity and hence osteoblast numbers, and (c) directly reduces osteoblast numbers. In addition to inducing severe, resistant osteomalacia, aluminum appears to contribute to the mild osteomalacia commonly seen in renal failure, characterized by extensive thin osteoid and low tetracycline and osteoblast surfaces.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405308
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  • 35
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    Electronic Resource
    Respiratory alkalosis and reduced plasmatic concentration of ionized calcium in rats treated with 1,25 dihydroxycholecalciferol (1984)
    Springer
    Calcified tissue international 36 (1984), S. 604-607 
    Details
    ISSN: 1432-0827
    Keywords: Respiratory alkalosis ; Ionized calcium ; 1,25 Dihydroxycholecalciferol ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The daily administration of supraphysiological doses of 1,25 dihydroxycholecalciferol (0.1–2.5 µg/d/100 g body weight) to rats, produced respiratory alkalosis. With the doses of 0.1–0.2 µg/d/100 g and feeding a diet with 0.7% of calcium, calcemias did not exceed 2.75 mM, and significantly reduced plasma ionized calcium levels were measured. The latter phenomenon was found associated with increased urinary excretion of cAMP, soft tissue calcium content, and polyuria with hypostenuria, all known effects of parathyroid hormone. These effects were absent in thyroparathyroidectomized rats treated in the same fashion. Present results suggest that the stimulus of low levels of plasma ionized calcium overcomes the probably inhibitory effect of the steroid on parathyroid hormone secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405374
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