Korean J Physiol Pharmacol.
1999 Aug;3(4):415-425.
Different mechanisms for K+-induced relaxation in various arteries
- Affiliations
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- 1Department of Physiology and Biophysics, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Gu, Seoul, 110-799 South Korea.
Abstract
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(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.