Cadnapaphornchai P, Boykin J, Harbottle J A, McDonald K M, Schrier R W
Am J Physiol. 1975 Jan;228(1):155-9. doi: 10.1152/ajplegacy.1975.228.1.155.
In the present study the effect of angiotensin II (AII) on renal water excretion was evaluated. In dogs undergoing a water diuresis, neither the intravenous (IV) (40ng/kg per min) nor intracarotid (5-10 ng/kg per min) infusion of AII significantly altered urinary osmolality (Uosm) or free-water clearance (CH2O). Intravenous infusion of a competitive inhibitor of AII (1-sarcosine,8-glycine AII) into hydropenic dogs also failed to alter Uosm and CH2O significantly. To examine whether AII might suppress, rather than stimulate, vasopressin release, AII was also infused into hydropenic animals. No effect on Uosm and CH2O was observed during the intracarotid infusion. A significant fall in Uosm and rise in CH2O occurred during the intravenous AII infusion, but reversal after cessation of the infusion was incomplete and statistically not significant. Some suppression of antidiuretic hormone (ADH) release during the intravenous infusion of AII, however, was suggested since no similar alteration in renal water excretion was observed during an intravenous AII infusion in hypophysectomized animals receiving a constant infusion of ADH. Taken together, the present results provide no evidence for a direct effect of AII to alter ADH release or to interfere with the peripheral action of ADH. Suppression of ADH release may sometimes occur with pressor doses of intravenous angiotensin, but this effect is clearly less consistent than previously observed with intravenous norepinephrine.
在本研究中,评估了血管紧张素II(AII)对肾脏水排泄的影响。在进行水利尿的犬中,静脉内(IV)(40 ng/kg每分钟)或颈内(5 - 10 ng/kg每分钟)输注AII均未显著改变尿渗透压(Uosm)或自由水清除率(CH2O)。向限水犬静脉内输注AII的竞争性抑制剂(1 - 肌氨酸,8 - 甘氨酸AII)也未能显著改变Uosm和CH2O。为了研究AII是否可能抑制而非刺激血管升压素释放,还将AII输注到限水动物体内。颈内输注期间未观察到对Uosm和CH2O的影响。静脉内输注AII期间出现Uosm显著下降和CH2O升高,但输注停止后的逆转不完全且在统计学上不显著。然而,静脉内输注AII期间提示抗利尿激素(ADH)释放有一定抑制,因为在持续输注ADH的垂体切除动物静脉内输注AII期间未观察到肾脏水排泄有类似改变。综上所述,目前的结果没有提供证据表明AII对改变ADH释放或干扰ADH的外周作用有直接影响。静脉注射血管紧张素的升压剂量有时可能会抑制ADH释放,但这种作用明显不如先前静脉注射去甲肾上腺素时观察到的那样一致。