Berecek K H, Mah S C, Baum P, Hofbauer K G
J Hypertens Suppl. 1984 Dec;2(3):S29-31.
The mean arterial pressure (MAP) and heart rate (HR) responses to intracerebroventricular (i.c.v.) administration of arginine vasopressin (AVP) in unanaesthetized normotensive control and DOCA-salt hypertensive rats were studied. Intracerebroventricular administration of AVP (0.25-1000 ng) to control rats produced dose-dependent long-lasting increases in MAP (5-45 mmHg) and HR (35-110 beats/min). Peripheral treatment of rats with an antipressor AVP antagonist had no effect on i.c.v. AVP-induced increases in MAP and HR, whereas the responses were blocked by i.c.v. administration of the antagonist. Peripheral administration of phentolamine and propranolol also completely blocked the changes in MAP and HR. DOCA-salt hypertensive rats showed significantly greater increases in MAP and HR in response to i.c.v. AVP and a tenfold lower threshold for stimulation. The results demonstrate that AVP acting on central neural structures can produce increases in MAP and HR by stimulating sympathetic outflow. Increased sensitivity and responsiveness to i.c.v. AVP in hypertensive rats suggest a potential mechanism of action of AVP in hypertension.
研究了在未麻醉的正常血压对照大鼠和去氧皮质酮盐（DOCA）-盐高血压大鼠中，脑室内（i.c.v.）注射精氨酸加压素（AVP）后平均动脉压（MAP）和心率（HR）的反应。向对照大鼠脑室内注射AVP（0.25 - 1000 ng）可使MAP（5 - 45 mmHg）和HR（35 - 110次/分钟）产生剂量依赖性的持久升高。用抗降压AVP拮抗剂对大鼠进行外周处理，对i.c.v. AVP诱导的MAP和HR升高没有影响，而脑室内注射拮抗剂可阻断这些反应。外周注射酚妥拉明和普萘洛尔也完全阻断了MAP和HR的变化。DOCA-盐高血压大鼠对i.c.v. AVP的反应显示MAP和HR升高明显更大，且刺激阈值低十倍。结果表明，作用于中枢神经结构的AVP可通过刺激交感神经传出而使MAP和HR升高。高血压大鼠对i.c.v. AVP的敏感性和反应性增加提示了AVP在高血压中的潜在作用机制。
