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Different Mechanisms for K+-Induced Relaxation in Various Arteries
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  • Different Mechanisms for K+-Induced Relaxation in Various Arteries
저자명
SukHyoSuh,SungJinPark,JaiYoungChoi,JaeHoonSim,YoungChulKim,KiWhanKim
간행물명
The Korean Journal of Physiology & PharmacologyKCI,SCI,SCOPUS
권/호정보
1999년|3권 4호(통권16호)|pp.415-425 (11 pages)
발행정보
대한생리학회-대한약리학회|한국
파일정보
정기간행물|ENG|
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영문초록

[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 was provoked 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 μM) 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.

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