Hyperkalemia alters endothelium-dependent relaxation through non -nitric oxide mechanism in porcine coronary arteries: a new mechanism for coronary dysfunction. He, Guo-Wei, Cheng-Qin Yang, Wolfgang Graier, Jan-An Yang. Cardiovascular Research Laboratory, The Grantham Hospital, Department of Surgery, University of Hong Kong, Hong Kong and Cardiovascular Research Laboratories, The Albert Starr Academic Center for Cardiac Surgery, St. Vincent Hospital, Portland, Oregon, U.S.A., University of Graz, Austria
APStracts 3:0094H, 1996.
Hyperkalemic solutions are widely used to preserve organs for transplantation and for cardiac surgery. The present study was designed to test the hypothesis that hyperkalemia may alter endothelial function through non-nitric oxide (NO) pathway since preliminary studies have shown that this pathway may not be affected. Porcine coronary artery rings were studied in organ chambers. After incubation with 20 or 50 mM K+ for one hour, the indomethacin- and L -NNA-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced. Incubation with hyperkalemia also significantly increased EC50 to A23187 and bradykinin. A23187-induced hyperpolarization of the membrane potential was significantly reduced by the hyperkalemia-incubation. However, one-hour incubation with hyperkalemia does not affect the endothelial Ca2+ concentration. We conclude that exposure to hyperkalemia reduces the indomethacin- and L-NNA-resistant, endothelium-dependent relaxation and the endothelium-dependent hyperpolarization. This reduction of the relaxation and the hyperpolarization is related to the endothelium -derived hyperpolarizing factor by affecting its effect on the smooth muscle cell, probably through partially depolarizing the membrane and affecting the KCa channels, and rather than by affecting its biosynthesis/release in the endothelial cell. Our study may suggest a new mechanism for coronary dysfunction after exposure to hyperkalemic cardioplegia and organ preservation solutions. 

Received 31 May 1995; accepted in final form 7 February 1996.
APS Manuscript Number H504-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96