PubMed1991
1. To characterize further the K+ channels opened by cromakalim in arterial smooth muscle, the effects of cromakalim on tension and 86Rb efflux were compared in endothelium-denuded strips of coronary, mesenteric and middle cerebral (MC) arteries of the dog. 2. Cromakalim relaxed strips precontracted with 20.9 mM K+. The maximum relaxation induced by cromakalim varied in the arteries used; 94% in the coronary artery, 60% in the mesenteric artery and only 38% in the MC artery. Cromakalim failed to relax arterial strips precontracted with 65.9 mM K+. 3. When the effects of cromakalim on 86Rb efflux were determined in 20.9 mM K(+)-contracted strips, cromakalim-induced relaxations were accompanied by a large increase in 86Rb efflux in the coronary artery, by a small increase in the mesenteric artery but by an apparent decrease in the MC artery. 4. When 10(-7) M nifedipine was added to 20.9 mM K(+)-contracted strips, to inactivate Ca2(+)-activated K+ (KCa) channels, cromakalim produced a greater increase (measured from the point at which cromakalim was administered) in 86Rb efflux than in the absence of nifedipine, suggesting that the effects of cromakalim on 86Rb efflux from the 20.9 mM K(+)-contracted strips may be the resultant of two opposing effects: an increased 86Rb efflux perhaps due to the opening of ATP-sensitive K+ (KATP) channels, and a decreased efflux due to the closing of KCa channels. 5. After the inactivation of Kca channels in 20.9mM K+-contracted strips, the cromakalim-induced increase in 86Rb efflux measured as area under the curve was eight times greater in the coronary artery than in the MC artery. The increase in 86Rb efflux in the mesenteric artery was intermediate between these extremes. 6. Cromakalim also increased the 86Rb efflux from 65.9 mm K+-contracted strips. This increase was not augmented by the addition of nifedipine. Under these conditions, a similar variation in efflux response (as area under the curve) for cromakalim was noted in the arteries used. 7. The relaxant responses of each artery to cromakalim were competitively antagonized by glibenclamide, a blocker of KATP channels. The cromakalim-induced increase in 86Rb efflux was also inhibited by glibenclamide. 8. These results suggest that cromakalim-opened K+ channels in the three arteries may differ in terms of their frequency of occurrence in the plasmalemma, their permeability to 86Rb and their ability to modulate tension development. On the other hand, the activities of Kca and voltage-sensitive K+ channels, estimated from the effects of nifedipine, were similar in the three arteries.