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[Myocardial beta adrenergic receptors in experimental renal hypertension, type Goldblatt II].

作者信息

Gende O A, Camilión de Hurtado M C, Taquini C M, Gómez Llambí H, Cingolani H E

出版信息

Acta Physiol Pharmacol Latinoam. 1985;35(1):57-65.

PMID:2865867
Abstract

Properties of cardiac beta-adrenergic receptors from two kidney-one clip hypertension and control rats were studied to determine whether or not alterations in the receptor contribute to the decreased responsiveness of two kidney-one clip rat hearts to adrenergic stimulation. The number and affinity of the beta-receptors were assessed by the binding of [3H]DHA in an enriched ventricular membrane fraction obtained from the rat hearts 3 and 4 weeks after the application of the clip. In the rats with 3 weeks of development of hypertension no significant difference was found neither in the number nor in the affinity of receptors (30.9 +/- 5.3 fmol/mg protein, KD: 1.62 +/- 0.43 nM) compared to the control rats (33.3 +/- 6.3 fmol/mg protein, KD: 2.21 +/- 0.59 nM). In rats with 4 weeks of development of hypertension, there was an increased number of receptors (54.7 +/- 3.7 fmol/mg protein, KD: 1.41 +/- 0.17 nM) compared with control rats studied in paralleled conditions (40.0 +/- 2.3 fmol/mg protein, KD: 1.13 +/- 0.12 nM). These results suggest that the reported beta-adrenergic subsensitivity in this model of hypertensive rats could be mediated by a biochemical mechanism other than a direct alteration of the beta adrenergic receptors, and that there is a compensatory increase in the density of receptors during the development of the hypertension.

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