FOREARM ENDOTHELIUM-DEPENDENT VASCULAR-RESPONSES AND THE POTASSIUM-ATP CHANNEL

Aims Vasodilation to acetylcholine is mediated at least in part by end othelium-derived hyperpolarising factor (EDHF) which causes membrane h yperpolarisation by activating potassium channels. It is however uncer tain which potassium channel mediates this effect. The aim of this stu dy was to determine the role of the potassium-ATP (K+-ATP) channel in mediating endothelium-deyendent vascular responses to acetylcholine. M ethods In 10 healthy volunteers acetylcholine, an endothelium-dependen t vasodilator, and sodium nitroprusside as a control assessing endothe lium-independent vasodilatation were infused into the non-dominant bra chial artery. Forearm blood flow (FBF) in response to each dose was me asured by strain-gauge venous occlusion plethysmography. The K+-ATP ch annel blocker glipizide (2.5 mg) was then administered orally. After 4 5 min the infusions with FBF measurements were repeated. Results Acety lcholine (P < 0.01) and sodium nitroprusside (P < 0.01) both caused an increase in FBF. There was no significant difference in vascular resp onses to acetylcholine (P > 0.05) or sodium nitroprusside (P > 0.05) f ollowing K+-ATP channel blockade. Conclusions The K+-ATP channel does not modulate forearm arteriolar endothelium-dependent responses in hea lthy volunteers and therefore does not play a role in membrane hyperpo larisation.