Regulation of norepinephrine release by peripheral α2-receptor stimulation

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Abstract
Evidence obtained in animals and in vitro supports the existence of an .alpha.-receptor-mediated inhibitory regulation of norepinephrine [NE] release, the importance of such a system in man is not established. NE release was physiologically stimulated by change of posture and dynamic exercise in subjects while they were infused with phenylephrine, a predominant .alpha.1-receptor agonist, .alpha.-methylnorepinephrine, a predominant .alpha.2-agonist, and saline. Agonist infusions were administered at rates that induced a slight elevation in supine systolic pressure and at nonpressor rates. Agonist concentrations that induced much the same pressor responses (.alpha.1) were assumed on the basis of in vitro experiments to differ substantially in their affinity for .alpha.2-receptors. The hemodynamic response and the increase of plasma NE induced by changes in posture and exercise were of the same order during infusions of .alpha.-methylnorepinephrine, phenylephrine and saline. Similar results from the nonpressor as from pressor agonist infusions suggested that baroreflex-induced reduction in sympathetic neuronal activity had not confounded the results. Correction of plasma concentrations for individual values of NE clearance provided an index of NE release into the circulation that was not changed by phenylephrine or .alpha.-methylnorepinephrine. These results raise the question of the importance of peripheral .alpha.2-receptors in the regulation of NE release in man.