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血管紧张素II对离体抗利尿激素释放作用的中枢作用位点定位

Localization of central sites of action of angiotensin II on ADH release in vitro.

作者信息

Gregg C M, Malvin R L

出版信息

Am J Physiol. 1978 Feb;234(2):F135-40. doi: 10.1152/ajprenal.1978.234.2.F135.

Abstract

It is now thought that angiotensin II can stimulate antidiuretic hormone (ADH) release in vivo by a direct action in the central nervous system but it is not known whether the locus of stimulation is the hypothalamus or the neurohypophysis or both. Isolated rat neural lobes incubated for 10 min in buffer containing angiotensin II (200 ng/ml or 2 microgram/ml) did not increase ADH release compared to control values, but addition of KCl (60 mM) to the bath markedly stimulated ADH release. However, intact hypothalamoneurohypophysial systems (containing the supraoptic nuclei) incubated with angiotensin II (200 ng/ml or 2 microgram/ml) did show a pronounced stimulation of ADH release. The data support the hypothesis that angiotensin II, at least in vitro, has a central effect on ADH release which is at the level of the hypothalamus.

摘要

现在认为,血管紧张素II可通过在中枢神经系统的直接作用在体内刺激抗利尿激素(ADH)释放,但刺激位点是下丘脑、神经垂体还是两者尚不清楚。与对照值相比,在含有血管紧张素II(200 ng/ml或2 μg/ml)的缓冲液中孵育10分钟的离体大鼠神经叶并未增加ADH释放,但向浴中添加氯化钾(60 mM)可显著刺激ADH释放。然而,用血管紧张素II(200 ng/ml或2 μg/ml)孵育的完整下丘脑-神经垂体系统(包含视上核)确实显示出ADH释放的明显刺激。这些数据支持以下假设:血管紧张素II至少在体外对ADH释放具有中枢作用,作用位点在下丘脑水平。

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