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终板血管器中的血管紧张素II受体而非穹窿下器中的血管紧张素II受体介导异丙肾上腺素诱发的口渴。

Angiotensin II receptors in SFO but not in OVLT mediate isoproterenol-induced thirst.

作者信息

Fitts D A

机构信息

Department of Psychology, University of Washington, Seattle 98195.

出版信息

Am J Physiol. 1994 Jul;267(1 Pt 2):R7-15. doi: 10.1152/ajpregu.1994.267.1.R7.

DOI:10.1152/ajpregu.1994.267.1.R7
PMID:8048647
Abstract

Thirst elicited by the beta-adrenergic agonist isoproterenol in rats depends in part on the secretion of renin, the consequent synthesis of angiotensin II (ANG II), and the binding of circulating ANG II to dipsogenic receptors in the brain. These receptors probably reside in either of two forebrain circumventricular organs, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT). Experiments determined that lesions of the SFO, but not of the OVLT, reduced drinking induced by isoproterenol treatment. Competitive ANG II-receptor antagonism with sarthran reduced isoproterenol-induced drinking when the blocker was infused into the SFO but not when it was infused into the OVLT or into the lateral ventricles at a 25-fold greater dose. The findings confirm the widely held belief that renin-dependent thirst elicited by isoproterenol relies on ANG II binding to receptor sites at a circumventricular organ in the brain. The results demonstrate that this site is the SFO and not the OVLT.

摘要

β-肾上腺素能激动剂异丙肾上腺素在大鼠中引发的口渴部分取决于肾素的分泌、随后血管紧张素II(ANG II)的合成,以及循环中的ANG II与大脑中致渴受体的结合。这些受体可能位于两个前脑室周器官中的一个,即穹窿下器官(SFO)或终板血管器(OVLT)。实验确定,SFO损伤而非OVLT损伤会减少异丙肾上腺素治疗引起的饮水。当将拮抗剂沙屈坦注入SFO时,其对ANG II受体的竞争性拮抗作用会减少异丙肾上腺素诱导的饮水,但当以高25倍的剂量注入OVLT或侧脑室时则不会。这些发现证实了人们普遍持有的观点,即异丙肾上腺素引发的肾素依赖性口渴依赖于ANG II与大脑中一个室周器官的受体位点结合。结果表明,这个位点是SFO而非OVLT。

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