Hackenthal E, Aktories K, Jakobs K H
Mol Cell Endocrinol. 1985 Sep;42(2):113-7. doi: 10.1016/0303-7207(85)90098-x.
Angiotensin II can elicit cellular responses by 2 different receptor-dependent mechanisms: increase in intracellular calcium or inhibition of adenylate cyclase activity. The well-known inhibition of renin release from granulated cells of the kidney is thought to be mediated by an increase in intracellular calcium. However, the participation of the other possible pathway, i.e. inhibition of adenylate cyclase, has not been excluded. We studied this question by using the toxin from Bordetella pertussis, which inactivates the inhibitory coupling units Ni and thus permits to identify hormonal actions mediated through inhibition of adenylate cyclase. In isolated perfused kidneys from rats pretreated with pertussis toxin (2 micrograms/100 g i.v., single injection) the inhibition of renin release by angiotensin II (10(-11) to 10(-8) M) was significantly attenuated. In parallel, the vasoconstrictor response to angiotensin II was also diminished in these rat kidneys. The effect of pertussis toxin was apparent 3, 5 and 10 days after treatment, with a maximal effect at the fifth day. These data suggest that angiotensin II may exert the inhibitory effect on renin release in part through inhibition of adenylate cyclase in granulated cells of the kidney.
血管紧张素II可通过两种不同的受体依赖性机制引发细胞反应：细胞内钙增加或腺苷酸环化酶活性受到抑制。众所周知，肾脏颗粒细胞中肾素释放的抑制作用被认为是由细胞内钙增加介导的。然而，其他可能的途径，即腺苷酸环化酶的抑制作用的参与尚未被排除。我们通过使用百日咳博德特氏菌毒素来研究这个问题，该毒素可使抑制性偶联单位Ni失活，从而能够识别通过抑制腺苷酸环化酶介导的激素作用。在用百日咳毒素（2微克/100克静脉内注射，单次注射）预处理的大鼠分离灌注肾脏中，血管紧张素II（10^(-11)至10^(-8) M）对肾素释放的抑制作用明显减弱。同时，这些大鼠肾脏中对血管紧张素II的血管收缩反应也减弱。百日咳毒素的作用在治疗后3天、5天和10天明显，在第5天达到最大效果。这些数据表明，血管紧张素II可能部分通过抑制肾脏颗粒细胞中的腺苷酸环化酶对肾素释放发挥抑制作用。
