Potassium as an Electro-Metabolic Signal for Local Coronary Vasodilation in Response to Metabolism and Hypoxemia

This study was designed to test the hypothesis that K + serves as an in vivo signal coupling 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 and during increases in myocardial oxygen consumption (MVO 2 ; n = 7), or systemic hypoxemia (PaO 2 to ~30 mmHg; n = 7). Further mechanistic studies examined the effects of K ATP channel inhibition (intracoronary glibenclamide; 1-3 mg/min) on coronary venous [K + ] under normoxic and hypoxemic conditions (n = 4). Dobutamine increased coronary flow and MVO 2 ~3-fold but coronary venous [K + ] did not change. Hypoxemia increased coronary blood flow ~2-fold and coronary venous [K + ] ~30%, which mirrored the increase in arterial [K + ]. Hypoxemia-induced increases in coronary blood flow and coronary venous [K + ] were also unaffected by glibenclamide. These findings demonstrate that myocardial interstitial [K + ] does not serve to couple coronary blood flow to MVO 2 during physiologic increases in cardiac work or pathophysiologic reductions in PaO 2 . 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.