Epithelioid cells: membrane potential changes induced by substances influencing renin secretion.
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.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D001160:Arterioles / Q000187:drug effects; D002395:Catecholamines / Q000494:pharmacology; D015232:Dinoprostone; D004848:Epithelium / Q000187:drug effects* / Q000201:enzymology; D005260:Female; D006632:Histamine / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D011458:Prostaglandins E / Q000494:pharmacology; D011687:Purines / Q000494:pharmacology; D012083:Renin / Q000378:metabolism*
D002395:Catecholamines; D011458:Prostaglandins E; D011687:Purines; D000804:Angiotensin II; D001127:Arginine Vasopressin; D006632:Histamine; D012083:Renin; D015232:Dinoprostone