Physiological Differences between the Effects of Neuronally Released and Bloodborne Norepinephrine on Beta Adrenergic Receptors in the Arterial Bed of the Dog

This investigation was designed to define the role of the beta adrenergic receptors in the regulation of peripheral vascular resistance and to determine whether norepinephrine released from nerve terminals acts at the same receptor sites in the arterial bed as injected norepinephrine. In 34 anesthetized dogs the skinned hindlimb was perfused at a constant flow rate, and in 8 dogs a segment of the splanchnic vascular bed was similarly perfused through the aorta. The hemodynamic responses of the isolated perfused beds of control dogs were compared with those of dogs in which the alpha receptors had previously been blocked with phenoxybenzamine, thereby maximizing any contribution of the beta receptors. In the control animals, both carotid sinus hypotension and norepinephrine administered directly into the perfused segment increased vascular resistance. In those animals subjected to alpha-receptor blockade, carotid sinus hypotension still caused reflex vasoconstriction, though it was considerably attenuated, but intra-arterially injected norepinephrine produced vasodilation. Following subsequent beta-receptor blockade, no potentiation of reflex constriction occurred, although the response to injected norepinephrine reverted to constriction. These findings suggest that norepinephrine released from nerve terminals in the arterial tree does not produce physiologically significant beta-receptor stimulation; humorally transported norepinephrine, however, stimulates both alpha and beta receptors.