IN-VIVO REACTIVITY OF RESISTANCE ARTERIOLES TO ACTIVATION OF ATP-SENSITIVE K+ CHANNELS

Our goal was to examine in vivo responses of resistance arterioles con tained within the hamster cheek pouch microcirculation to activation o f ATP-sensitive potassium (K+) channels. We measured changes in diamet er of cheek pouch arterioles in response to activation of ATP-sensitiv e K+ channels using RP 52891 (Aprikalim) and BRL 38227 (active enantio mer of cromakalim). RP 52891 and BRL 38227 produced dose-related dilat ation of arterioles, which was inhibited by glibenclamide (1.0 muM), b ut not altered by N(G)-monomethyl-L-arginine (L-NMMA; 1.0 muM). Gliben clamide did not alter baseline diameter of cheek pouch arterioles and did not alter dilatation of cheek pouch arterioles in response to nitr oglycerin (1.0 and 10 muM). L-NMMA did not alter dilatation of arterio les to nitroglycerin, but inhibited dilatation of arterioles to acetyl choline (0.1, 1.0 and 10 muM). Thus, dilatation of arterioles in respo nse to activation of ATP-sensitive K+ channels appears to be specific and does not involve the release of nitric oxide or a nitric oxide con taining compound. The findings of the present study suggest that ATP-s ensitive K+ channels are functional in resistance arterioles in vivo, but do not appear to affect resting tone of cheek pouch arterioles.