Relaxation of coronary smooth muscle by dobutamine

Dobutamine, a non-selective β-adrenergic receptor agonist, is commonly used to increase cardiac output. While its primary actions are attributed to stimulation of cardiac muscle, dobutamine may also directly influence coronary vascular tone. We tested the hypothesis that dobutamine relaxes coronary smooth muscle, in part, through the activation of ATP-dependent (KATP) and Ca 2+ -activated K + (BK) channels. Left circumflex coronary artery rings were isolated from male and female Yorkshire swine and studied using isometric tension recording techniques. Rings were contracted with U46619 (a thromboxane A2 mimetic), and concentration-dependent relaxation responses to dobutamine were recorded. The role of the endothelium was evaluated by comparing responses in intact and denuded arteries, while K + channel involvement was assessed using PNU 37883 and penitrem A (blockers of KATP and BK channels, respectively). Dobutamine produced concentration-dependent relaxation of coronary arteries that was unaffected by endothelial removal, indicating effects were directly on smooth muscle. When hyperpolarization mechanisms were blocked by adding high extracellular K + , dobutamine-induced relaxation was cut in half, suggesting K + channels may be involved. Blocking BK channels with penitrem A had no effect on dobutamine-mediated relaxation; however, inhibition of KATP channels with PNU 37883 reduced relaxation by ~40%. These findings demonstrate that dobutamine directly relaxes coronary smooth muscle independent of the endothelium, likely through activation of KATP channels. This mechanism may contribute to the coronary vasodilation observed clinically during dobutamine administration. This abstract was presented at the American Physiology Summit 2026 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.