Impaired Hypoxic Coronary Vasodilation and ATP-Sensitive Potassium Channel Function

Hypoxic coronary vasodilation contributes to themaintenance of oxygen supply to the working heartduring increased metabolic demand. Mechanisms of hypoxic coronary dilation have been studied extensively and differ considerably depending upon the species and experi-mental model. In isolated coronary vessels, several mecha-nisms have been implicated either alone or in combination, including release of vasodilatory factors (ie, nitric oxide, prostaglandins, and adenosine), activation of ATP-sensitive potassium (KATP) channels and Ca2-activated K channels, and inhibition of voltage-gated Ca2 channels.1–5 To date, however, relatively few studies have been conducted in human blood vessels. Furthermore, whereas most prior stud-ies have examined hypoxic dilation in conduit coronary arteries, coronary microvessels (150 m in diameter) are considered to be the principal regulators of coronary blood flow in response to metabolic stress.6 Thus, despite extensive