Mayhan W G
Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha 68198.
Eur J Pharmacol. 1993 Sep 21;242(1):109-12. doi: 10.1016/0014-2999(93)90017-c.
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 microM), but not altered by NG-monomethyl-L-arginine (L-NMMA; 1.0 microM). 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 microM). L-NMMA did not alter dilatation of arterioles to nitroglycerin, but inhibited dilatation of arterioles to acetylcholine (0.1, 1.0 and 10 microM). 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 suggest that ATP-sensitive K+ channels are functional in resistance arterioles in vivo, but do not appear to affect resting tone of cheek pouch arterioles.
我们的目标是研究仓鼠颊囊微循环中阻力性小动脉对ATP敏感性钾（K+）通道激活的体内反应。我们使用RP 52891（阿普卡林）和BRL 38227（克罗卡林的活性对映体）来测量颊囊小动脉直径因ATP敏感性K+通道激活而发生的变化。RP 52891和BRL 38227可引起小动脉剂量相关的扩张，这种扩张被格列本脲（1.0微摩尔）抑制，但不受N-甲基-L-精氨酸（L-NMMA；1.0微摩尔）影响。格列本脲不改变颊囊小动脉的基线直径，也不改变颊囊小动脉对硝酸甘油（1.0和10微摩尔）的扩张反应。L-NMMA不改变小动脉对硝酸甘油的扩张，但抑制小动脉对乙酰胆碱（0.1、1.0和10微摩尔）的扩张。因此，ATP敏感性K+通道激活引起的小动脉扩张似乎具有特异性，且不涉及一氧化氮或含一氧化氮化合物的释放。本研究结果表明，ATP敏感性K+通道在体内阻力性小动脉中具有功能，但似乎不影响颊囊小动脉的静息张力。
