Blair-West J R, Coghlan J P, Denton D A, Niall H D, Scoggins B A, Tregear G W
Prog Biochem Pharmacol. 1976;12:53-62.
To test the role of the renin/angiotensin system in aldosterone regulation, Sar1-Ala8-angiotensin II (P113) was infused into the arterial blood supply of transplanted adrenal glands in conscious sheep. Effects on the aldosterone response to infused angiotensin II and III in sodium replete sheep were compared with effects in sodium deficiency. Adrenal arterial infusion of P113 up to 1,000 mug/h for 1-2h did not consistently alter the high aldosterone secretion rates of sodium-deficient sheep. However, infusion of P113 at 10 mug/h or more abolished aldosterone responses to angiotensin II infusion that caused high physiological blood levels of angiotensin II. These results are against the proposal of a primary proportional causal relationship between blood angiotensin II concentration and aldosterone secretion rate in sodium deficiency. They are also against the possibility that such a primary role is played by blood-borne angiotensin III.
为了测试肾素/血管紧张素系统在醛固酮调节中的作用,将Sar1-Ala8-血管紧张素II(P113)注入清醒绵羊移植肾上腺的动脉血供中。将钠充足的绵羊中P113对注入血管紧张素II和III时醛固酮反应的影响与钠缺乏时的影响进行比较。以高达1000微克/小时的速度向肾上腺动脉输注P113 1-2小时,并未持续改变钠缺乏绵羊的高醛固酮分泌率。然而,以10微克/小时或更高的速度输注P113会消除醛固酮对导致血管紧张素II生理血浓度升高的血管紧张素II输注的反应。这些结果与钠缺乏时血中血管紧张素II浓度与醛固酮分泌率之间存在主要比例因果关系的提议相悖。它们也排除了血源性血管紧张素III发挥这种主要作用的可能性。