Blockade of central angiotensin II type 1 and type 2 receptors suppresses adrenalectomy-induced NaCl intake in rats

被引：12

作者：

Galaverna, O ^{[1
]}

Polidori, C ^{[1
]}

Sakai, RR ^{[1
]}

Lienard, F ^{[1
]}

Chow, SY ^{[1
]}

Fluharty, SJ ^{[1
]}

机构：

[1] COLL FRANCE,LAB NEUROBIOL REGULAT,CNRS URA 1860,F-75231 PARIS 05,FRANCE

来源：

REGULATORY PEPTIDES | 1996年 / 66卷 / 1-2期

关键词：

losartan; PD; 123319; sodium appetite; AT1; AT2; aldosterone;

D O I：

10.1016/0167-0115(96)00062-6

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Removal of the adrenal glands, the main site for the synthesis of aldosterone, produces an intake of sodium that is essential for survival. Using central blockade of angiotensin II (Ang II) receptors with Sarlle Ang II, previous studies have shown that this intake depends on the stimulation of the brain angiotensin system. In the present study, using intracerebroventricular injection of specific antagonists of Ang II type 1 (AT1) or type 2 (AT2) receptors (losartan and PD 123319, respectively), we confirm that activation of brain angiotensin is essential for the expression of adrenalectomy-induced NaCl intake. Moreover, we show that (a) AT1 but not AT2 receptor blockade alone suppresses NaCl intake and (b) doses of AT1 and AT2 receptor antagonists that separately have no effect on NaCl intake, suppress the behavior when combined. It is proposed that AT1 receptors mediate the natriorexigenic effect of Ang II and that AT2 receptors have a permissive role on AT1 receptor stimulation.

引用

页码：47 / 50

页数：4

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