Neurohypophyseal Hormones and Analogues: Magnesium Dependence and Contraction of Arterial Smooth Muscle 1

Abstract

Summary

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 neurohypophyseal 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 [Mg²⁺]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 least one mammalian vascular muscle-rat aorta- is directly rather than inversely proportional to the rat pressor potency of the molecules. Further, the vaso-pressin receptor which subserves contraction in mammalian blood vessels may differ in this respect from that in uterine smooth muscle.

The author wishes to express his thanks to Miss Marjorie K. Nicodemus and Mr. C. F. Reich for their excellent technical assistance. The author is indebted to Dr. B. Berde (Sandoz Ltd.) and Dr. R. Walter (Mt. Sinai School of Medicine) for generously supplying the synthetic peptides used in this study.