Bührle C P, Scholz H, Hackenthal E, Nobiling R, Taugner R
Mol Cell Endocrinol. 1986 Apr;45(1):37-47. doi: 10.1016/0303-7207(86)90080-8.
Microelectrode recordings were performed in renin-containing epithelioid (JG) and vascular smooth muscle (VSM) cells of the afferent arteriole in the isolated hydronephrotic mouse kidney. Both cell types had a membrane potential of about -75 mV and exhibited small, spontaneous depolarizing transients, probably resulting from random transmitter release by sympathetic axon terminals. Substances depressing renin secretion, such as angiotensin II, arginine-vasopressin, and alpha 1-adrenergic agents reversibly depolarized both JG and VSM cells. On a molar basis, the action of angiotensin II was strongest. Stimulators of renin release, e.g. isoproterenol, histamine, and prostaglandin E2 did not influence the membrane potential of both cell types. VIP and NPY, possible co-transmitters of norepinephrine, as well as AP II, were also without effect. It is proposed that suppression of renin secretion from JG cells is mediated by depolarization and Ca2+ influx, whereas stimulation is triggered independently from membrane potential changes, e.g. by adenylate cyclase activation.
在分离的肾积水小鼠肾脏入球小动脉含肾素的类上皮（球旁）细胞和血管平滑肌细胞中进行微电极记录。两种细胞类型的膜电位均约为 -75 mV，并表现出小的、自发的去极化瞬变，这可能是由交感神经轴突终末随机释放递质所致。抑制肾素分泌的物质，如血管紧张素 II、精氨酸加压素和α1 - 肾上腺素能药物，可使球旁细胞和血管平滑肌细胞均发生可逆性去极化。按摩尔计算，血管紧张素 II 的作用最强。肾素释放的刺激剂，如异丙肾上腺素、组胺和前列腺素 E2 对两种细胞类型的膜电位均无影响。血管活性肠肽和神经肽 Y（去甲肾上腺素可能的共递质）以及血管紧张素 II 也无作用。有人提出，球旁细胞肾素分泌的抑制是由去极化和 Ca2+ 内流介导的，而刺激则独立于膜电位变化触发，例如通过腺苷酸环化酶激活。
