Objective--Experimental evidence indicates that ATP-sensitive potassium (K_ATP) channels regulate coronary blood flow (CBF). However, their contribution to human metabolic coronary vasodilation is unknown.

Methods and Results--Seventeen patients (12 mol/L, age 58±10 years) were studied. Coronary hemodynamics were assessed before and after K_ATP channel inhibition with subselective intracoronary glibenclamide infused at 40 µg/min in an angiographically smooth coronary artery after successful percutaneous coronary intervention to another vessel. Metabolic vasodilation was induced by 2 minutes of rapid right ventricular pacing. Coronary blood velocity was measured with a Doppler guidewire and CBF calculated. The time course of hyperemia was recorded for 2 minutes after pacing, and hyperemic volume was estimated from the area under the flow-versus-time curve (AUC). Compared with vehicle infusion (0.9% saline), glibenclamide reduced resting CBF by 9% (P=0.04) and increased resting coronary vascular resistance (CVR) by 15% (P=0.03). Glibenclamide reduced pacing-induced peak CBF (50.8±6.8 versus 42.0±5.4 mL/min, P=0.001), peak CBF corrected for baseline flow (25.1±4.6 versus 17.6±3.1 mL/min, P=0.01), and increased minimum CVR (2.6±0.3 versus 3.1±0.3 mm Hg/mL per minute, P=0.002). Compared with vehicle, glibenclamide reduced total AUC at 2 minutes (3535±397 versus 3027±326 mL, P=0.001).

Conclusions--Vascular K_ATP channels appear to be involved in functional coronary hyperemia after metabolic stimulation.