Impaired relaxation of the carotid artery during activation of ATP-sensitive potassium channels in atherosclerotic monkeys.

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Abstract
This study examined the hypotheses that (1) atherosclerosis impairs relaxation of the carotid artery in response to activation of adenosine triphosphate (ATP)-sensitive potassium channels and (2) regression of atherosclerosis restores the response toward normal. Isometric tension was measured in rings of carotid artery taken from normal, atherosclerotic, and regression monkeys and precontracted submaximally with prostaglandin F2 alpha. Relaxation in response to acetylcholine was less in atherosclerotic compared with normal arteries (5 +/- 6% versus 54 +/- 4% [mean +/- SE] in response to 3 x 10(-8) mol/L acetylcholine, P < .01). Relaxation in response to aprikalim, a direct activator of ATP-sensitive potassium channels, was also less in atherosclerotic than in normal arteries (32 +/- 7% versus 69 +/- 5% during 10(-6) mol/L aprikalim, P < .01). Relaxation in response to aprikalim but not to acetylcholine or nitroprusside was inhibited almost completely by glibenclamide (4 mumol/L), a selective inhibitor of ATP-sensitive potassium channels. Relaxation in response to low but not high (10(-6) to 10(-5) mol/L) concentrations of sodium nitroprusside was less in atherosclerotic than in normal arteries. Regression of atherosclerosis tended to restore responses to acetylcholine, but not responses to nitroprusside or aprikalim, toward normal. These findings suggest that atherosclerosis impairs relaxation of the carotid artery in response to activation of ATP-sensitive channels. Impaired responses may be due, in part, to nonspecific impairment of relaxation. Regression of atherosclerosis did not restore responses of the carotid artery toward normal.