THE ROLE OF ANGIOTENSIN, AT1-RECEPTOR AND AT2-RECEPTOR IN THE PRESSOR, DRINKING AND VASOPRESSIN RESPONSES TO CENTRAL ANGIOTENSIN
THE ROLE OF ANGIOTENSIN, AT1-RECEPTOR AND AT2-RECEPTOR IN THE PRESSOR, DRINKING AND VASOPRESSIN RESPONSES TO CENTRAL ANGIOTENSIN
复制标题
DOI：
10.1016/0006-8993(92)91638-u
复制
发表时间：
1992-07-24
期刊：
影响因子：
2.9
通讯作者：
PHILLIPS, MI
中科院分区：
文献类型：
--
作者：
HOGARTY, DC;SPEAKMAN, EA;PHILLIPS, MI
血管紧张素II（Ang II）集中给药会增加血压和饮酒的动机。介导升压反应的生理机制包括加压素（AVP）的释放和交感神经系统的激活。使用2个新的血管紧张素Ⅱ受体拮抗剂，我们能够调查的作用，AT 1或AT 2受体介导这些影响。将成年雄性Sprague-Dawley大鼠在侧脑室中插管，5天后在颈动脉中插管用于血压测量。所有实验均在清醒大鼠中进行。三种处理是心室内（i.v.t.），在2 μ l人工脑脊液（ACSF）中，以30分钟间隔：（1）50 ng Ang II，（2）0.7 μ g AT 1拮抗剂Losartan或7.0 μ g AT 2拮抗剂PD 123177，随后50 ng Ang II，和（3）50 ng Ang II，以测试恢复。记录血压和饮酒量。此外，在2个单独的大鼠组中，在注射后1或3分钟抽取用于测定AVP的血液样品。我们发现Losartan和PD 123177均显著减少注射后1 min AVP向Ang II的释放。氯沙坦显著阻断升压反应（P < 0.001），而PD 123177无明显作用。洛沙坦也能对抗饮酒（P < 0.05）并减少饮酒（n. s）PD123177结果提示，血管紧张素Ⅱ（i.v.t.）主要是AT 1介导的，而饮水和AVP反应可能由两种受体亚型介导。
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) and activation of the sympathetic nervous system. Using 2 new Ang II receptor antagonists, we were able to investigate the role of AT1 or AT2 receptors in mediating these effects. Adult male Sprague-Dawley rats were cannulated in the lateral ventricle and 5 days later catheterized in the carotid artery for blood pressure measurements. All experiments were carried out in conscious rats. Three treatments were given intraventricularly (i.v.t.), in 2-mu-l artificial cerebrospinal fluid (ACSF) at 30 min intervals: (1) 50 ng Ang II, (2) 0.7-mu-g AT1 antagonist Losartan or 7.0-mu-g AT2 antagonist PD123177, followed by 50 ng Ang II, and (3) 50 ng Ang II, to test for recovery. Blood pressure and drinking measurements were recorded. Also, blood samples for assay of AVP were drawn at 1 or 3 min post-injection in 2 separate groups of rats. We found that both Losartan and PD123177 significantly reduced release of AVP to Ang II 1 min post-injection. Losartan significantly blocked the pressor response (P < 0.001), while PD123177 had no significant effect. Drinking was also antagonized by Losartan (P < 0.05) and reduced (n.s.) by PD123177. The results suggest that the pressor response to Ang II (i.v.t.) is predominantly AT1 mediated, while the drinking and AVP responses may be mediated by both receptor subtypes.