Altered Vascular Response to the K+induced Vasorelaxation in Aortic Smooth Muscle of Renal Hypertensive Rats

Background:An increase of the extracellular K concentrations up to about 8 mM in the isolated vessels causes relaxation in pre-contracted state. In order to elucidate the mechanisms of K-induced relaxation and compare with that of 2-kidney, 1 clip (2K1C) renal hypertensive rats, we recorded aortic vascular tension using an organ bath study. Methods:2K1C hypertension was made by clipping the left renal artery and agematched control rats received a sham treatment. Thoracic aortic rings were mounted in tissue baths for measurement of isometric contractile force. Results:Exposure to K (from 2 to 8 mM) relaxed a phenylephrine (2×10 M)-induced contraction in K-free Krebs-Ringer solution, dose-dependently. Ouabain (10 M) enhanced the K-induced relaxation in above 2 mM K. The K-induced relaxation was still induced in endothelium-denuded condition. Incubation with the K channel blockers such as tetraethylammonium (TEA, 1 mM), glibenclamide(10 M), 4-aminopyridine (3 mM), barium (5 mM) and cesium (2 mM) did not affect on the K-induced relaxation. In renal hypertensive rats, the K-induced relaxation was markedly suppressed and ouabain enhanced it. Conclusions:These results suggest that the K-induced relaxation in aorta be mediated by Na-pump independent mechanisms, and the decrease of the K-induced relaxation in the renal hypertensive rats may be a possible mechanism of hypertension. . (Korean Circulation J 2000;30(8):980-988)