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Am J Physiol Heart Circ Physiol 284: H2405-H2411, 2003. First published February 21, 2003; doi:10.1152/ajpheart.00879.2002
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Vol. 284, Issue 6, H2405-H2411, June 2003

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

H. M. Omar Farouque and Ian T. Meredith

Cardiovascular Research Centre, Monash Medical Centre and Monash University, Melbourne 3168, Victoria, Australia

Isolated ATP-sensitive K+ (KATP) channel inhibition with glibenclamide does not alter exercise-induced forearm metabolic vasodilation. Whether forearm metabolic vasodilation would be influenced by KATP 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 NG-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 KATP channel blockade with glibenclamide does not affect resting FBF or FHBF in the setting of NO and vasodilator prostanoid inhibition.

blood flow; exercise hyperemia; ion channels; vasoregulation


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