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Am J Physiol Heart Circ Physiol (February 21, 2003). doi:10.1152/ajpheart.00879.2002
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Submitted on October 9, 2002
Accepted on February 6, 2003

Relative Contribution of Vasodilator Prostanoids, NO and ATP-sensitive K+ Channels to Human Forearm Metabolic Vasodilation

H. M. Omar Farouque1* and Ian T. Meredith1

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

* To whom correspondence should be addressed. E-mail: omar.farouque{at}med.monash.edu.au.

Isolated ATP-sensitive K+ channel inhibition with glibenclamide does not alter exercise-induced forearm metabolic vasodilation. Whether forearm metabolic vasodilation would be influenced by ATP-sensitive K+ channel inhibition in the setting of impaired 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) induced by isotonic wrist exercise. Infusion of L-NMMA, aspirin or the combination reduced resting FBF compared to vehicle (P<0.05). The 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 repaid after 5 minutes (P<0.05). Aspirin reduced peak FHBF by 13% and volume repaid after 5 minutes (P<0.05). Coinfusion of L-NMMA and aspirin reduced peak FHBF by 21% (P<0.01), and volume repaid after 5 minutes (P<0.05). Addition of glibenclamide to L-NMMA and aspirin did not further decrease FHBF. Vascular ATP-sensitive K+ channel blockade with glibenclamide does not affect resting FBF or FHBF in the setting of NO and vasodilator prostanoid inhibition.




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