ET(A) RECEPTOR-MEDIATED ROLE OF ENDOTHELIN IN THE KIDNEY OF DOCS-SALT HYPERTENSIVE RATS

被引：8

作者：

FUJITA, K ^{[1
]}

MATSUMURA, Y ^{[1
]}

MIYAZAKI, Y ^{[1
]}

HASHIMOTO, N ^{[1
]}

TAKAOKA, M ^{[1
]}

MORIMOTO, S ^{[1
]}

机构：

[1] OSAKA UNIV PHARMACEUT SCI,DEPT PHARMACOL,MATSUBARA,OSAKA 580,JAPAN

来源：

LIFE SCIENCES | 1995年 / 58卷 / 01期

关键词：

ENDOTHELIN-1; ET(A) RECEPTOR; DOCA-SALT HYPERTENSION; RENAL FUNCTION;

D O I：

10.1016/0024-3205(95)02259-7

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Renal effects of FR139317, an endothelin ETA receptor antagonist, were examined using anesthetized normotensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The intravenous bolus injection of FR139317 (10 mg/kg) produced a slight decrease in mean blood pressure (MAP; -13%) in the control rats and this hypotension was accompanied by a moderate renal vasodilation (renal vascular resistance: RVR; -12%). In the DOCA-salt hypertensive rat, FR139317 had a more pronounced hypotensive effect (MAP; -26%) accompanied by a potent renal vasodilation (RVR; -33%). FR139317 significantly increased renal blood flow only in the DOCA-salt rats. In contrast, FR139317 produced a significant decrease in urine flow and urinary sodium excretion only in control rats. Northern blot analysis revealed that the renal prepro endothelin-l (ET-1) mRNA level was significantly increased in DOCA-salt hypertensive rats. Thus, it seems likely that endogenous ET-1 is responsible for the maintenance of DOCA-salt-induced hypertension. We also suggest that at least in part, ET-1 and ETA receptors are involved in renal hemodynamic abnormalities in DOCA-salt-induced hypertension. The augmentation of renal ET-1 production may possibly have a function in the development and maintenance of DOCA-salt-induced hypertension.

引用

页码：PL1 / PL7

页数：7

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