Our goal was to examine in vivo responses of resistance arterioles contained within the hamster cheek pouch microcirculation to activation of ATP-sensitive potassium (K+) channels. We measured changes in diameter of cheek pouch arterioles in response to activation of ATP-sensitive K+ channels using RP 52891 (Aprikalim) and BRL 38227 (active enantiomer of cromakalim). RP 52891 and BRL 38227 produced dose-related dilatation of arterioles, which was inhibited by glibenclamide (1.0 μM), but not altered by NG-monomethyl-L-arginine (L-NMMA; 1.0 μM). Glibenclamide did not alter baseline diameter of cheek pouch arterioles and did not alter dilatation of cheek pouch arterioles in response to nitroglycerin (1.0 and 10 μM). L-NMMA did not alter dilatation of arterioles to nitroglycerin, but inhibited dilatation of arterioles to acetylcholine (0.1, 1.0 and 10 μM). Thus, dilatation of arterioles in response to activation of ATP-sensitive K+ channels appears to be specific and does not involve the release of nitric oxide or a nitric oxide containing compound. The findings of the present study suggests that ATP-sensitive K+ channels are functional in resistance arterioles in vivo, but do not appear to affect resting tone of cheek pouch arterioles.
- Cheek pouch arterioles
- L-NMMA (N-monomethyl-L-arginine)
- Nitric oxide (NO)
- Vasodilatation, BRL 38227
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