Role of ATP-Dependent Potassium Channels in Electro-Metabolic Signaling for Local Coronary Vasodilation

This study was designed to test the hypothesis that ATP-dependent K + (K ATP ) channels are an in vivo signal to couple coronary blood flow with the oxidative requirements of the myocardium. Experiments were performed in open-chest swine preparations in which coronary parameters and arterial and coronary venous [K + ] were measured under baseline conditions, in the presence of glibenclamide (a K ATP channel blocker), and in the presence of pinacidil (a K ATP channel opener). The left anterior descending coronary artery was cannulated and perfused with arterial blood at either a constant flow or constant pressure. In constant flow experiments to prevent ischemia, intracoronary glibenclamide dose-dependently (1-3 mg/min) increased coronary vascular resistance, but did not affect coronary venous [K + ]. In constant pressure experiments, intracoronary pinacidil (0.3-3 µg/kg/min) increased coronary blood flow in a dose-dependent manner, but did not change coronary venous [K + ]. These findings demonstrate that K ATP channels do not regulate interstitial [K + ] as a signal to control coronary vascular function. National Institutes of Health grant R01 HL158723 and theResearch Enhancement Program at UNTHSC This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.