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  • 1
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    Vitamin D deficiency in rats with normal serum calcium concentrations. (1982)
    National Academy of Sciences
    Details
    Publication Date: 1982-08-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Evidence for an important physiological role for calcitonin (1980)
    National Academy of Sciences
    Details
    Publication Date: 1980-01-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 3
    Electronic Resource
    Electronic Resource
    An interpretation of acute changes in plasma45Ca following parathyroid hormone administration to thyroparathyroidectomized rats (1977)
    Springer
    Calcified tissue international 22 (1977), S. 117-128 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Plasma calcium ; Radiocalcium ; Bone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract Acute changes in plasma calcium and45Ca were studied in young adult male thyroparathyroidectomized (TPTX) rats injected with moderate doses of parathyroid hormone (PTH). For plasma calcium changes, comparison was made between rats fasted or fed prior to PTH injection. For plasma45Ca changes, the effect of the time of administration of the radionuclide was also studied; this included rats injected with PTH 1 h after radionuclide (“1 h45Ca”), 18 h later (“18 h45Ca”) and more than 6 days later (“6 day45Ca”). The results can be summarized as follows: (1) Plasma calcium changes were greater when PTH was injected into “fed” rather than into “fasted” rats. (2) PTH always produced a relative increase (compared to controls tested concurrently) in plasma45Ca concentrations. This increase was the same in the “1 h45Ca” and the “18 h45Ca” groups. (3) Plasma45Ca rose at least temporarily following PTH injection in the “18 h45Ca” group. (4) The45Ca rise following PTH was always greater in “fed” than in “fasted” groups. (5) Plasma45Ca specific activities (S.A.) tended to rise in the “6 day45Ca” group and to fall in the “18 h45Ca” group, following PTH injection. However, the45Ca S.A. was always higher in fed than fasted groups. (6) In a few experiments in which32P was injected with45Ca, specific activity changes in plasma45Ca following PTH injection werenot accompanied by similar changes in32P specific activity. These results could not be adequately explained by PTH effects on bone resorption, but the data supported the postulate that PTH controls plasma calcium concentrations by increasing transport of calcium through the osteocyte-lining cell (osteoblast) bone cell complex from the bone fluid compartment to the ECF.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02010351
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    A reevaluation of the cause of acute hypercalcemia following intravenous administration of lead acetate (1978)
    Springer
    Calcified tissue international 26 (1978), S. 149-153 
    Details
    ISSN: 1432-0827
    Keywords: Lead ; Plasma calcium ; 45Ca ; Bone uptake of lead
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of intravenous (i.v.) injection of lead acetate (15 or 30 mg/kg) was studied in young adult male rats. The reaction of lead with rat plasma to produce colloidal material containing both calcium and phosphate was demonstrated both in vitro and in vivo. This material could be centrifuged down at 25,000 ×g from plasma aliquots to which lead had been added or from plasma samples obtained as early as 5 min after i.v. lead injection. The hypercalcemia and hyperphosphatemia reached their peak rapidly after lead injection, and even at the higher dose level these lasted less than 6 h.45Ca and32P were injected at times varying from 1 to 8 days prior to lead administration. Plasma radioactivity levels rose with their stable counterparts without affecting plasma nuclide specific activity. Lead uptake on bone surfaces could be detected within 5 min of injection, and continued to accumulate for at least 6 h. It is concluded that although lead attaches to bone surfaces, the hypercalcemia and hyperphosphatemia are caused by the direct interaction of lead with calcium and phosphate in solution in plasma. The formation of the colloidal material lowers ionic calcium and phosphate. In vivo, calcium and phosphate are immediately withdrawn from extravascular sources returning plasma concentrations to their initial value. The source of at least the calcium is believed to be bone. The attachment of lead to bone surfaces does not in itself release significant amounts of calcium and phosphate into blood.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02013250
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of salmon calcitonin infusion on plasma concentrations of recently administered45Ca (1977)
    Springer
    Calcified tissue international 24 (1977), S. 201-208 
    Details
    ISSN: 1432-0827
    Keywords: Calcitonin ; Plasma calcium ; Radiocalcium ; Bone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of intravenous salmon calcitonin (SCT) infusion on the net rate of loss from plasma of recently injected45Ca has been studied in conscious fasted rats, some of which had been previously thyroparathyroidectomized (TPTX). The45Ca was injected 10 h prior to or 1 or 2 h after the initiation of the infusion. Salmon calcitonin (0.05–0.2 MRC mU/g body weight/h) infusion produced the expected hypocalcemia and hypophosphatemia. The drop in plasma calcium levels produced by the hormone was lowered further by the addition of phosphate to the infusate. Plasma45Ca changes, during SCT infusion, followed a biphasic pattern when the radionuclide injection preceded SCT infusion by 10 h. During the first part of the infusion, the rate of loss of45Ca from plasma was greater in SCT-treated than in control rats. Later, this pattern reversed, and the rate of loss of45Ca from plasma became slower in SCT-treated animals. If45Ca was injected after SCT infusion was initiated only the second phase of the biphasic effect was observed; i.e., disappearance of45Ca from plasma was slower in SCT-infused than in control rats. These data are considered to support the hypothesis that rapid and opposing calcium fluxes exist between bone fluid and plasma, and that calcitonin acts by decreasing the calcium efflux from bone fluid. The calcium moved in this efflux system includes some that has only recently entered bone fluid from plasma. This is the explanation given for the initial decrease in plasma45Ca concentrations following SCT infusion. The reverse effect in the second phase can be explained as the result of a secondary reduction in calcium influx to bone fluid from plasma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02223317
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  • 6
    Electronic Resource
    Electronic Resource
    Factors affecting parathyroid hormone-induced hypophosphatemia and32P specific activity in thyroparathyroidectomized rats (1979)
    Springer
    Calcified tissue international 27 (1979), S. 239-246 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Calcium ; Plasma phosphate ; Bone phosphate ; Plasma32P ; Specific activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Plasma changes in calcium, phosphate, and their radionuclides were studied in thyroparathyroidectomized (TPTX) rats treated with parathyroid hormone (PTH) for 8 h, this treatment starting 10 h after injection of45Ca and32P. Prior to intravenous infusion or hourly injections of PTH (10 mU/g/h), rats were maintained in one of three ways: on an extended fast (24 h); on a partial fast (10 h); or provided with 10% glucose and 1% calcium lactate overnight as a substitution for solid food. The pattern of change for plasma calcium,45Ca, and45Ca specific activity (S.A.) produced by PTH was not affected by these dietary conditions. The changes in phosphate were as follows: During the experimental (8 h) period, the rate of loss of32P from plasma in control rats was proportional to the length of the fast. This suggests that32P was released into plasma during the experimental period proportional to the ready availability of soft tissue glucose. In rats on an extended fast, PTH was phosphaturic, hypophosphatemic, and increased the rate of loss of32P from plasma without affecting32P S.A. values. In rats fasted for only 10 h, PTH produced similar effects on plasma phosphate and plasma32P values, but also caused a significant fall in plasma32P S.A. After glucose and calcium lactate treatment, PTH-induced phosphaturia was temporarily lost and the marked hypophosphatemia was replaced with a slight hyperphosphatemia. Plasma32P values also rose slightly; therefore, no effect on32P S.A. was produced. It is concluded from these studies that as the result of the phosphaturia caused by PTH, the hypophosphatemia which is produced automatically changes the phosphate gradient between various body compartments, causing phosphate entry into plasma. The authors postulate that this phosphate entering plasma is withdrawn primarily from bone fluid and bone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02441192
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