Different Mechanisms for K<SUP>⁢</SUP>-Induced Relaxation in Various Arteries
Different Mechanisms for K<SUP>⁢</SUP>-Induced Relaxation in Various Arteries
- 대한생리학회-대한약리학회
- The Korean Journal of Physiology & Pharmacology
- 제3권 제4호
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1999.01415 - 425 (11 pages)
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<P> [K<SUP>⁢</SUP>]<SUB>o</SUB> can be increased under a variety of conditions including subarachnoid hemorrhage. The increase of [K<SUP>⁢</SUP>]<SUB>o</SUB> in the range of 5∼15 mM may affect tensions of blood vessels and cause relaxation of agonist-induced precontracted vascular smooth muscle (K<SUP>⁢</SUP>-induced relaxation). In this study, effect of the increase in extracellular K<SUP>⁢</SUP> concentration on the agonist-induced contractions of various arteries including resistant arteries of rabbit was examined, using home-made Mulvany-type myograph. Extracellular K<SUP>⁢</SUP> 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<SUP>⁢</SUP> 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<SUP>⁢</SUP> 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<SUP>⁢</SUP>-induced relaxation by the elevation from initial 6 to 12 mM was blocked by Ba<SUP>2⁢</SUP> (30 μM) and the relaxation by the elevation from 1 to 3 mM or from 3 to 6 mM was not blocked by Ba<SUP>2⁢</SUP>. In cerebral arteries, however, K<SUP>⁢</SUP>-induced relaxation by the elevation from initial 3 to 6 mM was blocked by Ba<SUP>2⁢</SUP>, whereas the relaxation by the elevation from 1 to 3 mM was not blocked by Ba<SUP>2⁢</SUP>. Ouabain inhibited all of the relaxations induced by the extracellular K<SUP>⁢</SUP> elevations in three different ways. In cerebral arteries, when extracellular K<SUP>⁢</SUP> was increased to 14 mM with 2 or 3 mM increments, almost complete relaxation was induced at 1 or 3 mM of initial K<SUP>⁢</SUP> concentration and slight relaxation occurred at 6 mM. TEA did not inhibit Ba<SUP>2⁢</SUP>-sensitive relaxation at all and NMMA or endothelial removal did not inhibit K<SUP>⁢</SUP>-induced relaxation. Most conduit arteries such as aorta, carotid artery, and renal artery were not relaxed by the elevation of extracellular K<SUP>⁢</SUP>. Among conduit arteries, trunk of superior mesenteric artery and basilar artery were relaxed by the elevations of [K<SUP>⁢</SUP>]<SUB>o</SUB>. These data suggest that K<SUP>⁢</SUP>-induced relaxation has two independent components, Ba<SUP>2⁢</SUP>-sensitive and Ba<SUP>2⁢</SUP>-insensitive one and there are different mechanisms for K<SUP>⁢</SUP>-induced relaxation in various arteries.
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