Forearm endothelium-dependent vascular responses and the potassium-ATP channel

Vasodilation to acetylcholine is mediated at least in part by endothelium-derived hyperpolarising factor (EDHF) which causes membrane hyperpolarisation by activating potassium channels. It is however uncertain which potassium channel mediates this effect. The aim of this study was to determine the role of the potassium-ATP (K(+)-ATP) channel in mediating endothelium-dependent vascular responses to acetylcholine.In 10 healthy volunteers acetylcholine, an endothelium-dependent vasodilator, and sodium nitroprusside as a control assessing endothelium-independent vasodilatation were infused into the non-dominant brachial artery. Forearm blood flow (FBF) in response to each dose was measured by strain-gauge venous occlusion plethysmography. The K(+)-ATP channel blocker glipizide (2.5 mg) was then administered orally. After 45 min the infusions with FBF measurements were repeated.Acetylcholine (P0.01) and sodium nitroprusside (P0.01) both caused an increase in FBF. There was no significant difference in vascular responses to acetylcholine (P0.05) or sodium nitroprusside (P0.05) following K(+)-ATP channel blockade.The K(+)-ATP channel does not modulate forearm arteriolar endothelium-dependent responses in healthy volunteers and therefore does not play a role in membrane hyperpolarisation.