Different mechanisms for K+-induced relaxation in various arteries .
- Author:
Suk Hyo SUH
1
;
Sung Jin PARK
;
Jai Young CHOI
;
Jae Hoon SIM
;
Young Chul KIM
;
Ki Wha KIM
Author Information
1. Department of Physiology and Biophysics, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Gu, Seoul, 110-799 South Korea.
- Publication Type:Original Article
- MeSH:
Aorta;
Arteries*;
Basilar Artery;
Blood Vessels;
Carotid Arteries;
Cerebral Arteries;
Mesenteric Artery, Superior;
Muscle, Smooth, Vascular;
Ouabain;
Relaxation*;
Renal Artery;
Subarachnoid Hemorrhage;
Tea;
Wasps
- From:The Korean Journal of Physiology and Pharmacology
1999;3(4):415-425
- CountryRepublic of Korea
- Language:English
-
Abstract:
(K+)o can be increased under a variety of conditions including subarachnoid hemorrhage. The increase of (K+)o in the range of 5 ~ 15 mM may affect tensions of blood vessels and cause relaxation of agonist-induced precontracted vascular smooth muscle (K+-induced relaxation). In this study, effect of the increase in extracellular K+ concentration on the agonist-induced contractions of various arteries including resistant arteries of rabbit was examined, using home-made Mulvany-type myograph. Extracellular K+ was increased in three different ways, from initial 1 to 3 mM, from initial 3 to 6 mM, or from initial 6 to 12 mM. In superior mesenteric arteries, the relaxation induced by extracellular K+ elevation from initial 6 to 12 mM was the most prominent among the relaxations induced by the elevations in three different ways. In cerebral arteries, the most prominent relaxation was produced by the elevation of extracellular K+ from initial 1 to 3 mM and a slight relaxation wasp rovoked by the elevation from initial 6 to 12 mM. In superior mesenteric arteries, K+-induced relaxation by the elevation from initial 6 to 12 mM was blocked by Ba2+ (30 muM) and the relaxation by the elevation from 1 to 3 mM or from 3 to 6 mM was not blocked by Ba2+. In cerebral arteries, however, K+-induced relaxation by the elevation from initial 3 to 6 mM was blocked by Ba2+, whereas the relaxation by the elevation from 1 to 3 mM was not blocked by Ba2+. Ouabain inhibited all of the relaxations induced by the extracellular K+ elevations in three different ways. In cerebral arteries, when extracellular K+ was increased to 14 mM with 2 or 3 mM increments, almost complete relaxation was induced at 1 or 3 mM of initial K+ concentration and slight relaxation occurred at 6 mM. TEA did not inhibit Ba2+/-sensitive relaxation at all and NMMA or endothelial removal did not inhibit K+-induced relaxation. Most conduit arteries such as aorta, carotid artery, and renal artery were not relaxed by the elevation of extracellular K+. Among conduit arteries, trunk of superior mesenteric artery and basilar artery were relaxed by the elevations of (K+)o. These data suggest that K+-induced relaxation has two independent components, Ba2+-sensitive and Ba2+-insensitive one and there are different mechanisms for K+-induced relaxation in various arteries.
