The contractile responses of helically cut rat aortic strips to neurohypophyseal hormones and synthetic analogues in the presence and absence of 1.2 mM external magnesium ions [Mg++]o was studied. These experiments demonstrate that 1) [Mg++]o potentiates the contractile actions of a variety of neurohypophyseal peptides on vascular smooth muscle. 2) [Mg++]o can alter both the ED50s (i.e., hormone-receptor affinities) and intrinsic activities (or maximum contractile responses) of these molecules on vascular muscle. 3) The amino acid moieties in positions 1, 2, 3, and 8 of the vasopressin molecule interact, differentially, with [Mg++] to produce contraction of vascular muscle. 4) The length of the side chain, and basicity, in position 8 of the vasopressin molecule are probably important in Mg potentiation in mammalian vascular muscle. 5) Interaction of Mg with an aromatic group in position 3 might be critical for potency of vasopressin hormones of mammalian vascular muscle; the ED50 for oxytocin is not shifted to lower concentrations in the presence of [Mg++]o. Collectively, these data suggest that Mg probably acts at more than one site in vascular smooth muscle in the production of neurohypophyseal peptide-activated contractions. In addition, the present findings indicate that the Mg dependence of these peptides on at least one vascular muscle, rat aorta, is a direct function of the rat pressor potency of the molecules.
- Copyright © 1975 by American Physiological Society