Endothelium Contributes to β-Adrenergic Relaxation in Rat Femoral Arteries Independently of Nitric Oxide and Prostaglandins

Our study investigated the role of the endothelium in β-adrenergic-mediated arterial relaxation in male and female Sprague Dawley rats (250-300 g). We hypothesized that the mechanical removal of the endothelium would blunt relaxation induced by dobutamine, a non-selective β agonist. Isometric tension was recorded from segments of femoral arteries using wire myography. Some segments had their endothelium denduded, while others were left intact to serve as controls. In a subset of segments with intact endothelium, Nω-Nitro-L-arginine methyl ester (L-NAME; 100 µM) and indomethacin (100 µM) were used to block the synthesis of nitric oxide and prostaglandins, respectively. All segments were pre-contracted with the α1 agonist phenylephrine (10 µM) before adding cumulative concentrations of dobutamine (10 nM to 100 µM). No sex differences were found. Endothelial denudation was confirmed using 100 µM acetylcholine, which relaxed intact but not denuded segments. L-NAME and indomethacin had no effect on dobutamine-induced relaxation, suggesting neither nitric oxide nor prostaglandins are mediators. In contrast, removal of the endothelium caused a significant rightward shift in the concentration-response curve. These preliminary data suggest that endothelium contributes to dobutamine-mediated vascular relaxation, perhaps by an unidentified endothelium-derived hyperpolarizing factor. 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.