Rowland N E, Fregly M J
Department of Psychology, University of Florida, Gainesville 32611-2065.
Pharmacol Biochem Behav. 1993 Mar;44(3):623-6. doi: 10.1016/0091-3057(93)90177-u.
The AT-1 receptor antagonist, losartan potassium, produced a large rise in plasma renin activity (PRA) after peripheral, but not intracerebroventricular (ICV), administration. Peripheral, but not ICV administration of losartan also augmented the release of renin induced by peripheral administration of the beta-adrenergic agonist, isoproterenol. The increase in PRA induced by losartan plus isoproterenol was greater than the sum of the increases in PRA induced by the individual treatments. There was, however, no significant enhancement of the hypotensive action of isoproterenol by peripherally administered losartan. The AT-2 receptor antagonist, PD 123319, produced no increase in PRA after either peripheral or ICV injection. However, peripheral injection of PD 123319 slightly increased PRA after peripheral administration of isoproterenol. The data are discussed in terms of the relationship between renin-angiotensin systems and fluid intake, with special reference to the failure of peripherally administered losartan to block isoproterenol-induced water intake.
血管紧张素Ⅱ1型受体（AT-1）拮抗剂氯沙坦钾经外周给药而非脑室内（ICV）给药后，可使血浆肾素活性（PRA）大幅升高。氯沙坦经外周而非ICV给药，也可增强外周给予β-肾上腺素能激动剂异丙肾上腺素所诱导的肾素释放。氯沙坦加异丙肾上腺素所诱导的PRA升高大于单独治疗所诱导的PRA升高之和。然而，外周给予氯沙坦对异丙肾上腺素的降压作用并无显著增强。血管紧张素Ⅱ2型受体（AT-2）拮抗剂PD 123319经外周或ICV注射后，PRA均未升高。然而，外周注射PD 123319可使外周给予异丙肾上腺素后的PRA略有升高。本文根据肾素-血管紧张素系统与液体摄入之间的关系对这些数据进行了讨论，特别提及外周给予氯沙坦未能阻断异丙肾上腺素诱导的水摄入。
