Eguchi T, Bravo E L
Am J Physiol. 1984 Sep;247(3 Pt 1):E336-42. doi: 10.1152/ajpendo.1984.247.3.E336.
The mechanism(s) by which intracerebroventricularly administered angiotensin II (ANG II) regulates aldosterone production was investigated in dogs with chronically implanted cannula into a lateral cerebroventricle. In salt-replete and salt-depleted dogs, artificial cerebrospinal fluid (CSF) with or without ANG II (1, 10, 100 ng X kg-1 X min-1) was infused intracerebroventricularly for 2 h under pentobarbital anesthesia. Artificial CSF produced no significant humoral changes. Intracerebroventricular ANG II decreased plasma renin activity and increased both ACTH and plasma cortisol in both groups but decreased plasma aldosterone (PA) only in salt-depleted dogs. Dexamethasone pretreatment during intracerebroventricular ANG II decreased PA further in salt-replete but not in salt-depleted dogs. Moreover, the fall in PA during intracerebroventricular ANG II in salt-depleted dogs was prevented when intravenous infusion of ANG II (10 ng X kg-1 X min-1) was given simultaneously to maintain circulating ANG II levels. We conclude that PA response to intracerebroventricular ANG II is mediated primarily through the renin-angiotensin system in the salt-depleted state; however, in the salt-replete state, ACTH assumes a more important role.
通过向慢性植入侧脑室插管的犬脑室内注射血管紧张素II（ANG II）来研究其调节醛固酮分泌的机制。在盐负荷充足和盐负荷不足的犬中，在戊巴比妥麻醉下向脑室内注入含或不含ANG II（1、10、100 ng·kg⁻¹·min⁻¹）的人工脑脊液（CSF）2小时。人工脑脊液未引起显著的体液变化。脑室内注射ANG II可降低两组犬的血浆肾素活性，并增加促肾上腺皮质激素（ACTH）和血浆皮质醇水平，但仅在盐负荷不足的犬中降低血浆醛固酮（PA）。在脑室内注射ANG II期间进行地塞米松预处理，可使盐负荷充足的犬的PA进一步降低，但对盐负荷不足的犬无效。此外，当同时静脉注射ANG II（10 ng·kg⁻¹·min⁻¹）以维持循环ANG II水平时，可防止盐负荷不足的犬在脑室内注射ANG II期间PA下降。我们得出结论，在盐负荷不足的状态下，PA对脑室内ANG II的反应主要通过肾素-血管紧张素系统介导；然而，在盐负荷充足的状态下，ACTH起更重要的作用。
