Activation of ATP-sensitive potassium channels contributes to reactive hyperemia in humans
Banitt, P.F.; Smits, P.; Williams, S.B.; Ganz, P.; Creager, M.A.
American Journal of Physiology 271(4 Pt 2): H1594-H1598
1996
ISSN/ISBN: 0002-9513 PMID: 8897956 Document Number: 462791
Activation of ATP-sensitive potassium (K-ATP) channels present on vascular smooth muscle cells causes membrane hyperpolarization and vasodilation. The purpose of this study was to determine whether K-ATP channels contribute to reactive hyperemia in humans. Accordingly, we studied the effect of tolbutamide, a K-ATP channel inhibitor, on reactive hyperemic forearm blood flow. Forearm blood flow was measured by venous occlusion plethysmography. Forearm ischemia was produced by inflating a sphygmomanometric cuff on the arm to suprasystolic pressures for 5 min. After cuff release, forearm blood flow was measured during the reactive hyperemic phase for 5 min. Tolbutamide (1 mM blood concentration, n = 6) did not affect basal (2.4 +- 0.2 to 2.2 +- 0.1 ml cntdot 100 ml-1 cntdot min-1) or peak reactive hyperemic forearm blood flow (21.9 +- 3.8 to 22.6 +- 2.9 ml cntdot 100 ml-1 cntdot min-1, each P = NS), but it significantly attenuated total hyperemic volume (12.6 +- 1.7 vs. 9.2 +- 1.8 ml/100 ml, P lt 0.02). Vehicle (n = 6) did not affect basal flow, peak reactive hyperemic flow, or total hyperemia. To determine whether adenosine or endothelium-derived nitric oxide contribute to reactive hyperemia via K-ATP channels, adenosine (1.5-500 mu-g/min, n = 6) and acetylcholine (30 mu-g/min, n = 6) were infused before and during tolbutamide coinfusion. Tolbutamide did not significantly alter the forearm blood flow response to either adenosine or acetylcholine. In conclusion, K-ATP channels contribute to vasodilation during reactive hyperemia in humans.