作者: David C. Hogarty , Elisabeth A. Speakman , Viviana Puig , M. Ian Phillips
DOI: 10.1016/0006-8993(92)91638-U
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摘要: Angiotensin II (Ang II) given centrally produces an increase in blood pressure and motivation to drink. The physiological mechanisms that mediate the pressor response include release of vasopressin (AVP) activation sympathetic nervous system. Using 2 new Ang receptor antagonists, we were able investigate role AT1 or AT2 receptors mediating these effects. Adult male Sprague-Dawley rats cannulated lateral ventricle 5 days later catheterized carotid artery for measurements. All experiments carried out conscious rats. Three treatments intraventricularly (i.v.t.), μl artificial cerebrospinal fluid (ACSF) at 30 min intervals: (1) 50 ng II, (2) 0.7 μg antagonist Losartan 7.0 PD123177, followed by (3) test recovery. Blood drinking measurements recorded. Also, samples assay AVP drawn 1 3 post-injection separate groups We found both PD123177 significantly reduced post-injection. blocked (P < 0.001), while had no significant effect. Drinking was also antagonized 0.05) (n.s.) PD123177. results suggest (i.v.t.) is predominantly mediated, responses may be mediated subtypes.