Role of nitric oxide in systemic hemodynamic responses to dobutamine, epinephrine, and amrinone

Abstract

This study was designed to investigate the extent to which the systemic vasodilator effects of dobutamine, epinephrine, and amrinone are modulated by the endothelium-derived relaxing factor, nitric oxide (NO). This was a prospective study of low and high doses of the agonists before and after inhibition of NO synthesis. Experiments were performed in the basic research laboratories of the Center for Anesthesiology Research. Pentobarbital-anesthetized, intact Sprague-Dawley rats were studied in seven separate groups of eight rats each. The systemic vasodilator responses to the agonists were assessed before and after the administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester. Decreases in systemic vascular resistance in response to dobutamine and epinephrine were not observed after inhibition of NO synthesis, whereas the decrease in systemic vascular resistance in response to amrinone was still apparent. The results suggest that dobutamine and epinephrine produce systemic vasodilation through the release of NO, whereas amrinone produces vasodilation independent of NO release.