Magnesium-neurohypophyseal hormone interactions in contraction of vascular smooth muscle.

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.