Thunhorst R L, Johnson A K
Department of Psychology, University of Iowa, Iowa City 52242.
Am J Physiol. 1993 Jan;264(1 Pt 2):R211-7. doi: 10.1152/ajpregu.1993.264.1.R211.
These experiments examined the dipsogenic responses of rats to intracerebroventricularly administered angiotensin II (ANG II) under normotensive and hypotensive conditions. Intravenous infusion of the vasodilator drug minoxidil (25 micrograms.kg-1.min-1), combined with the angiotensin converting enzyme inhibitor captopril (0.33 mg/min), both reduced blood pressure and prevented endogenous ANG II formation. Central infusions with ANG II (4 or 16 ng/h) began 60 min later, and the intravenous and intracerebroventricular infusions ran concurrently for another 90 min. Mean arterial pressure (MAP), water intake, urine volume (UV) and electrolyte excretion were measured throughout. Water intakes to both doses of intracerebroventricular ANG II were increased, and UV and electrolyte excretion were reduced during hypotensive conditions compared with normotensive conditions. Thus the increased water intakes occurred despite increased fluid retention. It is concluded that arterial hypotension enhances the dipsogenic effects of centrally administered ANG II, possibly through baroreceptor-mediated mechanisms.
这些实验研究了在正常血压和低血压条件下,大鼠对脑室内注射血管紧张素II(ANG II)的致渴反应。静脉输注血管扩张剂米诺地尔(25微克·千克-1·分钟-1),并联合血管紧张素转换酶抑制剂卡托普利(0.33毫克/分钟),既能降低血压,又能阻止内源性ANG II的形成。60分钟后开始脑室内注射ANG II(4或16纳克/小时),静脉注射和脑室内注射同时持续90分钟。全程测量平均动脉压(MAP)、饮水量、尿量(UV)和电解质排泄量。与正常血压条件相比,在低血压条件下,两种剂量的脑室内ANG II引起的饮水量均增加,而UV和电解质排泄量减少。因此,尽管液体潴留增加,但饮水量仍增加。研究得出结论,动脉低血压可能通过压力感受器介导的机制增强脑室内注射ANG II的致渴作用。