Woodcock E A, Johnston C I
Endocrinology. 1982 Nov;111(5):1687-91. doi: 10.1210/endo-111-5-1687.
Adenylate cyclase of rat renal cortex was inhibited by angiotensin II (AII). Inhibition required Na+ (100-200 mM) and GTP (10(-8)-10(-4) M) and was opposed by the receptor antagonist [1-sarcosine, 8-isoleucine]AII. The EC50 value (+/- SE)for inhibition by AII was 3.7 +/- 1.2 nM, and the maximum inhibition (+/- SE) was 23 +/- 3%. Inhibition was specific for AII, since both AI and AIII, at concentrations up to 1 microM, were ineffective in producing inhibition. The maximum decrease (+/- SE) in adenylate cyclase activity was from 2.45 +/- 0.08 to 1.78 +/- 0.1 pmol.min/mg protein. A similar absolute decrease was observed when adenylate cyclase was stimulated by calcitonin, vasopressin, or isoproterenol. The inhibition of PTH-stimulated activity [16.7 +/- 0.5 (+/- SE) to 12.2 +/- 0.7 pmol.min/mg protein) was significantly greater than the inhibition of basal activity. Therefore, at least some of the inhibitory angiotensin receptors are coupled to adenylate cyclase molecules which also coupled to receptors for PTH.
大鼠肾皮质的腺苷酸环化酶受到血管紧张素II（AII）的抑制。抑制作用需要Na+（100 - 200 mM）和GTP（10^(-8) - 10^(-4) M），且受体拮抗剂[1-肌氨酸，8-异亮氨酸]AII可对抗这种抑制。AII抑制的EC50值（±SE）为3.7 ± 1.2 nM，最大抑制率（±SE）为23 ± 3%。抑制作用对AII具有特异性，因为浓度高达1 μM的AI和AIII均无法产生抑制作用。腺苷酸环化酶活性的最大降低值（±SE）从2.45 ± 0.08降至1.78 ± 0.1 pmol·min/mg蛋白质。当腺苷酸环化酶受到降钙素、血管加压素或异丙肾上腺素刺激时，也观察到了类似的绝对降低。甲状旁腺激素刺激的活性抑制（从16.7 ± 0.5（±SE）降至12.2 ± 0.7 pmol·min/mg蛋白质）明显大于基础活性的抑制。因此，至少部分抑制性血管紧张素受体与也与甲状旁腺激素受体偶联的腺苷酸环化酶分子相连。
