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Am J Physiol Heart Circ Physiol 284: H711-H718, 2003. First published December 12, 2002; doi:10.1152/ajpheart.00315.2002
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Vol. 284, Issue 2, H711-H718, February 2003

Inhibition of vascular ATP-sensitive K+ channels does not affect reactive hyperemia in human forearm

H. M. Omar Farouque and Ian T. Meredith

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

The extent to which ATP-sensitive K+ channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K+ channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced (n = 9). The contribution of vascular ATP-sensitive K+ channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K+ channel inhibitor (n = 12). To document ATP-sensitive K+ channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K+ channel opener, was undertaken (n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K+ channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.

regional blood flow; ion channels; ischemia


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