Flow-Induced Dilation of Human Coronary Arterioles

Background—Flow-induced vasodilation (FID) is a physiological mechanism for regulating coronary flow and is mediated largely by nitric oxide (NO) in animals. Because hyperpolarizing mechanisms may play a greater role than NO in the microcirculation, we hypothesized that hyperpolarization contributes importantly to FID of human coronary arterioles. Methods and Results —Arterioles from atria or ventricles were cannulated for videomicroscopy. Membrane potential of vascular smooth muscle cells (VSMCs) was measured simultaneously. After constriction with endothelin-1, increases in flow induced an endothelium-dependent vasodilation. Nv-Nitro-L-arginine methyl ester 10 24 mol/L modestly impaired FID of arterioles from patients without coronary artery disease (CAD), whereas no inhibition was seen in arterioles from patients with CAD. Indomethacin 10 25 mol/L was without effect, but 40 mmol/L KCl attenuated maximal FID. Tetraethylammonium 10 23 mol/L but not glibenclamide 10 26 mol/L reduced FID. Charybdotoxin 10 28

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