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  • 1
    Electronic Resource
    Electronic Resource
    Isoprenaline-induced increase in the 40/41 kDa pertussis toxin substrates and functional consequences on contractile response in rat heart (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 345 (1992), S. 44-50 
    Details
    ISSN: 1432-1912
    Keywords: Gi-protein ; Force of contraction ; β-Adrenoceptor ; Isoprenaline infusion ; Rat heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Chronic β-adrenoceptor stimulation leads to desensitization of the myocardial adenylyl cyclase signalling pathway which includes β-adrenoceptor downregulation and upregulation of Gi-protein α-subunits. However, these investigations have mainly been done in cellular preparations. In this study we report that isoprenaline infusion in vivo leads to an increase in myocardial Gia and present evidence for functional consequences of this increase. Rats were treated by a 4-day subcutaneous infusion with isoprenaline (2.4 mg/kg·d), propranolol (9.9 mg/kg·d) and triiodothyronine (T3, 0.5 mg/kg·d) for comparison. Isoprenaline treatment increased the pertussis toxin-sensitive amount of Gia by 22±6% and decreased β1- and β2-adrenoceptor density from 35±4 to 23±6 fmol/mg protein and 24±4 to 8±6 fmol/mg protein, respectively. Contraction experiments on electrically driven papillary muscles revealed that the negative inotropic potency of the M-cholinoceptor agonist carbachol in the presence of isoprenaline was increased as compared to control (mean EC50-values: 0.04 μmol/l vs. 0.28 μmol/l). All isoprenaline-induced effects were antagonized by simultaneously administered propranolol. T3 treatment had no influence on the parameters investigated. The results suggest that chronic β-adrenoceptor stimulation desensitizes myocardial adenylyl cyclase by at least two mechanisms: β-adrenoceptor downregulation leading to diminished signal transduction in the stimulatory pathway and Giα upregulation leading to sensitization of the inhibitory pathway. Such adaptation might protect the heart from chronic exposure to catecholamines in heart diseases with elevated plasma catecholamine levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175468
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Depletion of endogenous dopamine stores and shift in β-adrenoceptor subtypes in cardiac tissue following five weeks of chronic denervation (1998)
    Springer
    Molecular and cellular biochemistry 183 (1998), S. 215-219 
    Details
    ISSN: 1573-4919
    Keywords: heart ; denervation ; catcholamines ; β-adrenoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Surgical ablation of extrinsic cardiac nerve fibers results in a chronically denervated state of the left ventricle of the heart. The present study was performed to elucidate the effect of a period of five weeks of chronic denervation on cardiac catecholamine levels in general and dopamine in particular. Moreover, the possible effect on cardiac β-adrenoceptor subtypes was investigated. Experiments were performed on adult dogs. In addition to adrenaline and noradrenaline the tissue levels of dopamine were found to be severely depressed. A significant shift from β1- to β2-adrenoceptor subtype was observed, while the total β-adrenoceptor density remained unaffected. The present findings indicate that catecholamine synthesis in chronically denervated hearts is impaired upstream of dopamine and that a shift in β-adrenoceptor subtype occurs already within a relatively short period of five weeks of denervation, and suggest that the lack of endogenous catecholamines influence the relative expression levels of the two subtypes of β-adrenoceptors present in cardiac tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006861112530
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  • 3
    Electronic Resource
    Electronic Resource
    Distinct down-regulation of cardiac β1- and β2-adrenoceptors in different human heart diseases (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 217-220 
    Details
    ISSN: 1432-1912
    Keywords: Cardiac β-adrenoceptor subtypes ; Human myocardium ; Heart diseases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cardiac β-adrenoceptor density and β1- and β2-subtype distribution were examined in human left ventricular myocardium from transplant donors serving as controls and from patients with mitral valve stenosis, aortic valve stenosis, idiopathic dilated cardiomyopathy, and ischaemic cardiomyopathy respectively. The total β-adrenoceptor density was similar in transplant donors and patients with moderate heart failure (NYHA II–III) due to mitral valve stenosis, but was markedly reduced in all forms of severe heart failure (NYHA III–IV) studied. A reduction of both β1- and β2-adrenoceptors was found in patients with severe heart failure due to mitral valve stenosis or ischaemic cardiomyopathy. In contrast, a selective down-regulation of β1-adrenoceptors with unchanged β2-adrenoceptors and hence a relative increase in the latter was observed in idiopathic dilated cardiomyopathy and aortic valve stenosis. It is concluded that the extent of total β-adrenoceptor down-regulation is related to the degree of heart failure. Selective loss of β1-adrenoceptors is not specific for idiopathic dilated cardiomyopathy but also occurs in aortic valve stenosis. Changes in β1- and β2-subtype distribution are rather related to the aetiology than to the clinical degree of heart failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168613
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    Paper (German National Licenses)
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