[Modulation of electrical responses of endothelial cells by nicotinic cholinoreceptors].Fiziol Zh. 2009; 55(2):17-23.FZ
Because the sustained component of hyperpolarization of endothelial cells evoked by acetylcholine in isolated rat aorta may partially be mediated by the reversed Na(+)-Ca(2+) exchanger and Na(+)-K(+) ATPase, the mechanisms which transport Na(+) out of cells, we compared the electrical responses of endothelial cells from isolated rat aorta to acetylcholine with other Ca(2+) mobilizing agents and studied the effect of nicotine on endothelial membrane potential in order to asses the functional activity of nicotinic cholinoreceptors. Ca(2+) ionophores A23187 and ionomycin, as well as inhibitors of endoplasmic reticulum Ca(2+) ATPase cyclopiazonic acid and 2,5-di-tert-butylhydroquinone evoked a short-lived hyperpolarization which turned to a sustained depolarization of endothelial cells, a time course that substantially differed from that evoked by acetylcholine. Nicotine evoked a Na+ dependent depolarization of endothelial cells confirming functional activity ofnicotinic cholinoreceptors in rat aortic endothelial cells. The results suggest that stimulation of Na+ permeant nicotinic receptors by acetylcholine may contribute to sustained hyperpolarizatiom via stimulation of Na+ extrusion mechanisms.