Kelly C, Wholohan T, Yesberg N E
Q J Exp Physiol. 1983 Apr;68(2):161-6. doi: 10.1113/expphysiol.1983.sp002708.
Mildly dehydrated conscious Merino ewes were infused with vasopressin (AVP) at 5 mu x min-1 alone and simultaneously with the angiotensin II receptor blocker sar1ala8-angiotensin II (saralasin) at 15 micrograms x min-1. AVP was slightly pressor and produced an increase in the calculated total peripheral resistance, and an increase in glomerular filtration rate, urine flow and electrolyte excretion, without a change in total renal plasma flow. These results indicate renal efferent arteriolar vasoconstriction as well as other non-renal vasoconstriction. Saralasin infusion checked the rise in total peripheral resistance (which continued to increase after saralasin withdrawal), but caused a marked increase in renal vascular resistance resulting in a decrease in renal plasma flow and to a lesser extent in glomerular filtration rate. These results suggest that saralasin was acting as an angiotensin II agonist in the kidney, but as an antagonist elsewhere. Deductions from previous experiments in the literature of the renal function of angiotensin II, based on its supposed inhibition by saralasin, may not be justified.
对轻度脱水的清醒美利奴母羊,单独以5 微单位/分钟的速度输注血管加压素(AVP),并同时以15微克/分钟的速度输注血管紧张素II受体阻滞剂沙拉新(sar1ala8 - 血管紧张素II,saralasin)。AVP有轻微的升压作用,使计算出的总外周阻力增加,肾小球滤过率、尿流量和电解质排泄增加,而肾血浆总流量无变化。这些结果表明存在肾出球小动脉血管收缩以及其他非肾血管收缩。输注沙拉新抑制了总外周阻力的升高(在撤掉沙拉新后总外周阻力仍继续升高),但导致肾血管阻力显著增加,从而使肾血浆流量减少,肾小球滤过率也有一定程度降低。这些结果提示,沙拉新在肾脏中作为血管紧张素II激动剂起作用,但在其他部位则作为拮抗剂。基于以往文献中沙拉新对血管紧张素II的假定抑制作用而对血管紧张素II肾功能所做的推断可能并不合理。