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  • 1
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    Stuttgart : Bundesanstalt für Geowissenschaften und Rohstoffe
    Associated volumes
    Call number: K 94.0033 ; K 93.0010/CC8726
    In: Geologische Übersichtskarte
    Branch Library: GFZ Library
    Branch Library: GFZ Library
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  • 2
    ISSN: 0303-7207
    Keywords: afferent glomerular arteriole ; angiotensin II ; epithelioid cells ; junctional transmission ; renin ; vascular smooth muscle cells
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1041
    Keywords: Key words Metoprolol ; Cardiomyopathy ; G-proteins; β-adrenoceptor density
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: In human heart failure downregulation of β-adrenoceptors and upregulation of Gi-protein α-subunits (Giα) results desensitization of the myocardial β-adrenergic signal transduction pathway and reduced positive inotropic effects of catecholamines. Metoprolol treatment has been shown to restore the reduced β-adrenoceptor density in dilated cardiomyopathy. The main objective of the present study was to investigate whether metoprolol also decreases the elevated inhibitory Giα levels in patients suffering from congestive heart failure. Methods: Total Giα was determined by pertussis toxin-catalysed ADP ribosylation and β1- and β2-adrenoceptor densities by radioligand binding in right ventricular myocardial biopsies of 18 patients with dilated or ischaemic cardiomyopathy (NYHA II–IV) before and after 3 months of therapy. Nine controls were treated with conventional therapy only [diuretics, digitalis, nitrates, angiotensin-converting enzyme (ACE) inhibitors], and nine received the β1-selective blocker metoprolol in addition (mean 98 ± 12 mg daily). Results: In biopsies from patients treated with metoprolol, Giα significantly decreased to 74% of predrug value and total β-adrenoceptor increased by a selective increase in β1- adrenoceptors (44.7 vs 34.0 fmol ⋅ mg−1 protein). These effects were accompanied by significantly increased oxygen uptake at the anaerobic threshold (8.65 vs 6.95 ml ⋅ kg−1⋅ min−1). In the control group no significant changes in biochemical and clinical parameters occurred. Conclusion: Metoprolol partly reverses Giα-upregulation and β-adrenoceptor downregulation in heart failure, which might contribute to the clinical improvement of patients treated with β-blockers.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1041
    Keywords: Keywords Digoxin ; Amiodorone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1041
    Keywords: Adrenoceptors ; cardiomyopathy ; human myocardium ; β1- ; β2-adrenoceptors ; idiopathic dilated cardiomyopathy ; ischaemic cardiomyopathy ; receptor downregulation ; heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Total β-adrenoceptor density and β1- and β2-subtype distribution in right and left atria and in different ventricular regions from 14 failing and seven nonfailing human hearts have been compared. End-stage heart failure was due to idiopathic dilated cardiomyopathy (n=8) or ischaemic cardiomyopathy (n=6). In nonfailing hearts the total β-adrenoceptor density was similar in the right and left atria and in all the ventricular regions studied (about 70 to 80 fmol/mg protein). The β1:β2-adrenoceptor ratio in both nonfailing atria was similar (about 70:30%) and was significantly smaller than in the different regions of both ventricles (about 80:20%). The β1-subtype density was similar in nonfailing atria and ventricles (about 55 fmol/mg protein). The β2-subtype density was significantly higher in the right and left atrium (about 25 fmol/mg protein) than in both ventricles (about 15 fmol/mg protein). In patients with end-stage heart failure due to idiopathic dilated cardiomyopathy or ischaemic cardiomyopathy the total β-adrenoceptor density was reduced by 50–60% in all regions. On the other hand, the β1- and β2-subtype distribution differed with the cause of heart failure. In patients with idiopathic dilated cardiomyopathy, the β1-adrenoceptor density was lower in all regions, but the β2-adrenoceptor density was not significantly reduced. In patients with ischaemic cardiomyopathy both β1- and β2-adrenoceptors were reduced in all regions. It is concluded that downregulation of β-adrenoceptors in patients with end-stage idiopathic dilated cardiomyopathy or ischaemic cardiomyopathy occurs uniformly throughout the heart. The results support the hypothesis that changes in β-adrenoceptor subtypes may be related to the cause of heart failure.
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  • 6
    ISSN: 1432-1041
    Keywords: Captopril ; Dilated cardiomyopathy ; ACE-inhibitors ; G-proteins ; β-adrenoceptor density
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract In end-stage heart failure due to idiopathic dilated cardiomyopathy β1-adrenoceptors are downregulated and G1α-proteins are upregulated. The aim of the present study was to investigate the influence of the angiotensin-converting enzyme inhibitor captopril on β-adrenoceptor density and Giα-proteins in sequential endomyocardial biopsies. Nineteen patients with mild to moderate congestive heart failure due to idiopathic dilated cardiomyopathy (NYHA Class II–III) were studied before and after 8–11 weeks of therapy. Patients were randomised into a captopril and a control group; 9 patients received captopril 12.5–50 mg per day, (divided in 2–3 doses) p.o. in addition to “conventional” therapy with digoxin and diuretics, and 10 controls received “conventional” therapy only. Echocardiography, spiroergometry, right heart catheterisation and endomyocardial biopsies were performed before (baseline) and after treatment. Compared to baseline, captopril increased total β-adrenoceptor density by selectively increasing β1-adrenoceptors (31.6 vs 41.2 fmol·mg−1; p〈0.05) but had no significant effect on Giα-proteins. The results indicate that treatment with angiotensin-converting enzyme inhibitors partly restores myocardial β1-adrenoceptor density, and this action effect may contribute to the clinical improvement of patients with idiopathic dilated cardiomyopathy treated in this way.
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    The European physical journal 22 (1924), S. 222-227 
    ISSN: 1434-601X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1420-9071
    Keywords: 3-Isobutyl-1-methylxanthine ; guinea pig heart ; phosphodiesterase inhibitor ; isoprenaline ; slow inward current ; positive inotropic effect ; cAMP ; cGMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) mimicked the effects of isoprenaline on the force of contraction, the cAMP content and the slow Ca++ inward current (Isi) in isolated guinea pig papillary muscles. The results support the hypothesis that phosphodiesterase inhibitors and β-adrenoceptor agonists exert their positive inotropic effects by increasing Isi via the common mediator cAMP.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1420-9071
    Keywords: Hypoxia ; oxygen sensing ; erythropoietin ; isolated kidneys
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The glycoprotein hormone erythropoietin (EPO) counteracts tissue hypoxia by increasing the systemic oxygen-carrying capacity. It induces augmentation of red blood cell mass by stimulating the formation and differentiation of erythroid precursor cells in the bone marrow. EPO production is increased under various forms of diminished oxygen supply such as anemic or hypoxic hypoxia. In the adult organism, the kidneys are the major source of EPO. The precise nature of the cells responsible for renal EPO production, however, has not yet been elucidated. Most likely, peritubular cortical cells, e.g. interstitial or endothelial cells, are involved in the elaboration of the hormone. From the observation that isolated perfused rat kidneys produce EPO in an oxygen-dependent fashion we conclude that the ‘oxygen sensor’ that controls hypoxia-induced EPO synthesis is located in the kidney itself. Within the kidneys, the local venous oxygen tension which reflects the ratio of oxygen supply to oxygen consumption is measured and transformed into a signal that regulates the formation of EPO. However, the mechanism by which a decrease of oxygen delivery to the kidneys is linked to an enhanced EPO gene expression is not yet known. Two possible mechanisms of regulation are discussed: First, renal hypoxia could lead to enhanced formation of metabolic mediators, for example prostaglandins or adenosine, which might stimulate EPO gene transcription by increasing cellular levels of second messenger molecules. Second, some kind of molecular ‘oxygen receptor’ such as a heme protein, that controls EPO formation by an oxygen-dependent conformational change, could mediate signal transduction.
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  • 10
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary In isolated, electrically driven, left guineapig atria, theophylline (5×10−4 g/ml) increased the rate of45Ca uptake and release without affecting the total myocardial Ca content and the amount of exchangeable cellular Ca. In sheep and calf heart preparations, theophylline (10−4–10−3 g/ml) increased Ca inward current during excitation (as examined indirectly by Ca dependent changes of membrane potential in TTX-containing solutions) as well as tension development. It is concluded that the positive inotropic effect of theophylline in mammalian hearts is due to an increase in Ca influx during the excitation process.
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