Beta 1 Receptors Mediate Adrenergic Relaxation of the Rat Femoral Artery

The purpose of our study was to determine: a) the extent to which β adrenergic agonists relax vascular smooth muscle, b) the receptor type(s) that are activated; and c) the signaling mechanisms involved. Isometric tension was recorded from segments of rat femoral arteries. Arterial rings were stimulated with the α1 agonist phenylephrine (10 µM), which produced a stable contraction upon which mechanisms of relaxation were studied. Isoproterenol (10 nM to 10 µM), an agonist of β1 and β2 receptors, produced full relaxation. Dobutamine (10 nM to 10 µM), an agonist of β1 receptors, caused complete relaxation. Contracting arteries with 60 mM K + , which prevents membrane hyperpolarization, abolished β adrenergic relaxation. Neither 100 µM glibenclamide (an inhibitor of ATP-dependent K + channels), nor 1 mM 4-aminopyridine (an inhibitor of voltage-gated K + channels) affected β adrenergic relaxation. Ouabain (30 µM), an inhibitor of the Na + /K + -ATPase, blocked half of the β adrenergic relaxation. These data lead us to conclude that stimulation of β1 receptors fully antagonizes α1 adrenergic contraction through cellular mechanisms which activate the Na + /K + -ATPase. Research 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.