Di Nicolantonio R, Mendelsohn F A, Hutchinson J S, Takata Y, Doyle A E
Am J Physiol. 1982 May;242(5):R498-504. doi: 10.1152/ajpregu.1982.242.5.R498.
Chronic intracerebroventricular (icv) infusion of angiotensin II (ANG II) (6 micrograms/h) in rats resulted in a sustained 70-mmHg rise in blood pressure during 7 days of treatment. A marked dipsogenic response preceded the maximal rise in blood pressure, peaked at 24 h, and returned to control by the 5th day. Urinary sodium excretion rose on the 1st day of infusion but thereafter was not different from that of vehicle-infused rats. ANG II-infused rats showed a small but significant kaliuresis, a fall in serum osmolality (5.5 mosmol/kg), but no change in plasma Na+, K+, or glucose. Rats infused with the same dose of ANG II intravenously showed a small, 8-mmHg rise in blood pressure, but none of the changes noted after icv ANG II. Plasma renin activity was suppressed in rats infused with ANG II by both routes. We conclude that the pressor, dipsogenic, and renal excretory effects of icv ANG II are mediated centrally and cannot be explained by leakage of the peptide into the systemic circulation. Furthermore, the pressor and dipsogenic effects of ANG II become clearly dissociated during chronic icv infusion.
给大鼠慢性脑室内（icv）输注血管紧张素II（ANG II，6微克/小时），在治疗7天期间血压持续升高70 mmHg。在血压升至最高值之前出现明显的饮水增多反应，在24小时达到峰值，并在第5天恢复至对照水平。输注第1天尿钠排泄增加，但之后与输注赋形剂的大鼠无差异。输注ANG II的大鼠出现少量但显著的尿钾增多、血清渗透压降低（5.5毫摩尔/千克），但血浆Na⁺、K⁺或葡萄糖无变化。静脉输注相同剂量ANG II的大鼠血压小幅升高8 mmHg，但未出现icv输注ANG II后所观察到的任何变化。两种途径输注ANG II的大鼠血浆肾素活性均受到抑制。我们得出结论，icv ANG II的升压、致渴和肾脏排泄作用是由中枢介导的，不能用该肽漏入体循环来解释。此外，在慢性icv输注期间，ANG II的升压作用和致渴作用明显分离。
