STIMULATION OF NICOTINIC CHOLINORECEPTORS MODULATES ELECTRICAL RESPONSES OF ENDOTHELIAL CELLS
O.I. Bondarenko, V.F. Sagach
O.O. Bogomoletz Institute of Physiology, National AcademySciences of Ukraine, Kyiv, Ukraine
Abstract
Because the sustained component of hyperpolarization of endothelial cells evoked by acetylcholine in isolated rat aorta may partially be mediated by the reversed Na+-Ca2+ 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 Ca2+ mobilizing agents and studied the effect of nicotine on endothelial membrane potential in order to asses the functional activity of nicotinic cholinoreceptors. Ca2+ ionophores A23187 and ionomycin, as well as inhibitors of endoplasmic reticulum Ca2+ 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 of nicotinic 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.
Keywords:
endothelial cells, Na+-Ca2+ exchanger, Na+-K+ATPase
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