Kawashima K, Miwa Y, Fujimoto K
Gen Pharmacol. 1987;18(3):327-30. doi: 10.1016/0306-3623(87)90020-6.
Effects of physostigmine on heart rate, mean arterial pressure (MAP), plasma renin concentration (PRC) and vasopressin (AVP) release were investigated in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Physostigmine (100 micrograms/kg, i.a.) produced a greater and prolonged hypertensive response in the SHR than in the WKY. Heart rate was increased by physostigmine in SHR rats while it was unchanged in the WKY. PRC was unchanged or even slightly decreased in these animals when MAP was increased by physostigmine. An AVP pressor antagonist did not attenuate the pressor and cardiac effects of physostigmine in these animals. These data indicate that an impaired baroreflex mechanism or a different mode of sympathetic neuronal activation by physostigmine through the central mechanism appears to be contributory, at least in part, to the enhanced pressor responsiveness in the SHR. The renin-angiotensin system and AVP do not appear to be involved in the enhanced pressor responsiveness to physostigmine in SHR rats.
在自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）中研究了毒扁豆碱对心率、平均动脉压（MAP）、血浆肾素浓度（PRC）和血管加压素（AVP）释放的影响。毒扁豆碱（100微克/千克，腹腔注射）在SHR中产生的高血压反应比WKY更大且更持久。毒扁豆碱使SHR大鼠的心率增加，而WKY大鼠的心率则无变化。当毒扁豆碱使MAP升高时，这些动物的PRC未改变甚至略有下降。AVP升压拮抗剂并未减弱毒扁豆碱对这些动物的升压和心脏效应。这些数据表明，压力反射机制受损或毒扁豆碱通过中枢机制引起的交感神经元激活方式不同，似乎至少部分促成了SHR中升压反应性增强。肾素-血管紧张素系统和AVP似乎不参与SHR大鼠对毒扁豆碱升压反应性增强的过程。
