RENAL ALPHA-ADRENERGIC RECEPTORS AND GENETIC-HYPERTENSION

被引:12
作者
JACKSON, CA
INSEL, PA
机构
[1] Department of Pharmacology, 0636, University of California, San Diego, La Jolla, 92093-0636, CA
关键词
ALPHA-ADRENERGIC RECEPTORS; G PROTEINS; HYPERTENSION; SPONTANEOUSLY HYPERTENSIVE RATS; NA+H+ EXCHANGE; NA+K+-ATPASE;
D O I
10.1007/BF01213373
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
The hypothesis has been proposed that an increase in the number of renal alpha-adrenergic receptors may contribute to the pathogenesis of genetic hypertension. Herein we review recent findings regarding expression of renal alpha(1) (alpha(1a) , alpha(1b))- and alpha(2) (alpha(2a), alpha(2b))-adrenergic subtypes and we provide an updated revision of the above-stated hypothesis. Enhancement in receptor number or in post-receptor components responsible for alpha(1)- and alpha(2)-adrenergic mediated sodium reabsorption in proximal tubule may contribute to sodium retention and an elevation in blood pressure. Perhaps such changes contribute to the increase in blood pressure in genetically determined hypertension in humans, although direct tests of this notion have not yet been performed.
引用
收藏
页码:853 / 858
页数:6
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