Hackenthal E, Aktories K, Jakobs K H
Department of Pharmacology, University of Heidelberg, Federal Republic of Germany.
J Hypertens Suppl. 1985 Dec;3(3):S263-5.
Inhibition of renin release by angiotensin II (ANG II) is a calcium-dependent process and is thought to reflect the calcium-mobilizing action of ANG II observed in several tissues. However, in some tissues, such as liver and vascular smooth muscle, ANG II induces cellular responses through inhibition of adenylate cyclase. We examined the possibility that ANG II-induced inhibition of renin release from the kidney is also partly mediated through adenylate cyclase inhibition, by using pertussis toxin (PT), which selectively inactivates the coupling protein Ni, which couples inhibitory hormone receptors to adenylate cyclase. Rats were injected intravenously (i.v.) with 2 micrograms/100 g PT. In isolated kidneys, perfused in an open system with a synthetic medium 3, 5 and 10 days after PT treatment, the inhibition of renin release by ANG II as well as its vasoconstrictor response were significantly attenuated. This effect, which was most pronounced at lower concentrations of ANG II, indicates that ANG II may inhibit renin release partly through inhibition of adenylate cyclase activity.
血管紧张素II（ANG II）对肾素释放的抑制是一个依赖钙的过程，被认为反映了在多个组织中观察到的ANG II的钙动员作用。然而，在一些组织，如肝脏和血管平滑肌中，ANG II通过抑制腺苷酸环化酶诱导细胞反应。我们通过使用百日咳毒素（PT）来研究ANG II诱导的肾脏肾素释放抑制是否也部分通过腺苷酸环化酶抑制介导，PT能选择性地使将抑制性激素受体与腺苷酸环化酶偶联的偶联蛋白Ni失活。大鼠静脉注射（i.v.）2微克/100克PT。在PT处理后3、5和10天，用合成培养基在开放系统中灌注分离的肾脏，ANG II对肾素释放的抑制及其血管收缩反应均显著减弱。这种效应在较低浓度的ANG II时最为明显，表明ANG II可能部分通过抑制腺苷酸环化酶活性来抑制肾素释放。
