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腹侧前腹侧第三脑室的兴奋毒性损伤以及对中枢钠、哇巴因和血管紧张素II的升压反应。

Excitotoxic lesions of the ventral anteroventral third ventricle and pressor responses to central sodium, ouabain and angiotensin II.

作者信息

Veerasingham S J, Leenen F H

机构信息

Department of Medicine, University of Ottawa, Ont., Canada.

出版信息

Brain Res. 1997 Feb 21;749(1):157-60. doi: 10.1016/s0006-8993(96)01381-9.

Abstract

To clarify the role of neurones in the anteroventral third ventricle (AV3V) area in cardiovascular responses to CSF sodium, ouabain and angiotensin II (ANG II), we employed excitotoxic lesions of the ventral AV3V (vAV3V). In conscious lesioned Wistar rats with systemic vasopressin blockade, pressor and tachycardiac responses to intracerebroventricular (i.c.v.) artificial CSF containing 0.3 M NaCl or ouabain were significantly attenuated by 26-32% whereas responses to ANG II were not affected. Thus, in rats with systemic blockade of vasopressin mechanisms, the vAV3V region partially mediates acute pressor responses to i.c.v. sodium and ouabain but not to ANG II.

摘要

为阐明前腹侧第三脑室(AV3V)区域神经元在对脑脊液钠、哇巴因和血管紧张素II(ANG II)的心血管反应中的作用,我们采用了腹侧AV3V(vAV3V)的兴奋性毒性损伤。在系统性血管加压素阻断的清醒损伤Wistar大鼠中,对含0.3 M NaCl或哇巴因的脑室内(i.c.v.)人工脑脊液的升压和心动过速反应显著减弱了26%-32%,而对ANG II的反应未受影响。因此,在系统性阻断血管加压素机制的大鼠中,vAV3V区域部分介导了对i.c.v.钠和哇巴因的急性升压反应,但不介导对ANG II的反应。

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