Relative contribution of vasodilator prostanoids, NO, and KATP channels to human forearm metabolic vasodilation.

Isolated ATP-sensitive K(+) (K(ATP)) channel inhibition with glibenclamide does not alter exercise-induced forearm metabolic vasodilation. Whether forearm metabolic vasodilation would be influenced by K(ATP) channel inhibition in the setting of impaired nitric oxide (NO)- and prostanoid-mediated vasodilation is unknown. Thirty-seven healthy subjects were recruited. Forearm blood flow (FBF) was assessed using venous occlusion plethysmography, and functional hyperemic blood flow (FHBF) was induced by isotonic wrist exercise. Infusion of N(G)-monomethyl-l-arginine (l-NMMA), aspirin, or the combination reduced resting FBF compared with vehicle (P < 0.05). Addition of glibenclamide to l-NMMA, aspirin, or the combination did not further reduce resting FBF. l-NMMA decreased peak FHBF by 26%, and volume was restored after 5 min (P < 0.05). Aspirin reduced peak FHBF by 13%, and volume repaid after 5 min (P < 0.05). Coinfusion of l-NMMA and aspirin reduced peak FHBF by 21% (P < 0.01), and volume was restored after 5 min (P < 0.05). Addition of glibenclamide to l-NMMA and aspirin did not further decrease FHBF. Vascular K(ATP) channel blockade with glibenclamide does not affect resting FBF or FHBF in the setting of NO and vasodilator prostanoid inhibition.