Neurohypophyseal hormones and analogues: magnesium dependence and contraction of arterial smooth muscle.

The present quantitative results, using isolated rat aorta, demonstrate that different [Mg2+]o (i.e. 0.2, 1.2 and 6.0 mM) potentiate the contractile actions of a variety of neuohypophyseal hormones and synthetic analogues on vascular smooth muscle. [Mg2+]o can alter both the hormone-receptor affinities (H-RA) and intrinsic (contractile) activities (i.a.) of these peptides on vascular muscle; 1.2 mM [Mg2+]o (approximately that found in rat plasma) appears to optimize H-RA and i.a. on rat aortic smooth muscle. The presence of [Mg2+]o not only steepens the concentration-effect curves to the neurohypophyseal peptides but increases the maximum contractile responses as well. The present findings question that [Mg+]o potentiates responses to neurohypophyseal peptides by vascular muscle solely by affecting H-RA. The present study supports the notion that Mg2+ potentiates responses to these peptides by acting at sites other than the receptor in mammalian vascular muscle. In addition, the present experiments suggest that the [Mg2+]o dependence of neurohypophyseal peptides on at lesast one mammalian vascular muscle-rat aorta- is directly rather than inversely proportional to the rat pressor potency of the molecules. Further, the vasopressin receptor which subserves contraction in mammalian blood vessels may differ in this respect from that in uterine smooth muscle.