Effects and subcellular distribution of magnesium in smooth and striated muscle

Mg specifically increases the binding of neurohypophyseal peptides to smooth muscle membranes, and has some less well-defined effects on beta-adrenergic and other drug-induced responses of smooth muscle. The requirement of smooth muscle actomyosin for Mg is not significantly higher than that of the striated muscle proteins: maximal Ca activation can be obtained at about 1 mM [Mg2+]. This is comparable to the estimated free Mg2+ concentration in smooth muscle. The total Mg content of smooth muscle is approximately 30-35 mmol/kg dry cell wt, and approximately 50% of this can be removed in Mg-free solution. Mg concentration in mitochondria and in nuclei of rabbit portal anterior mesenteric vein smooth muscle is not significantly different from the cytoplasmic concentration. Mitochondria isolated from vascular smooth muscle have a highly active, energy-dependent Mg transport system. Mitochondria isolated from atherosclerotic bovine arteries contain increased concentrations of Mg and Ca. In the terminal cisternae of frog striated muscle tetanized for 12 s the Mg content is increased by 26 meq/kg dry wt, suggesting that there is an increase in the permeability of the sarcoplasmic reticulum membrane to (or transport of) Mg during tetanus. At this time, 126 meq Ca/kg dry terminal cisternae has been released, and there is a concomitant increase of 46 meq/kg dry wt K. The amount of Ca released during 1.2-s tetanus is sufficient to increase the total (not free) Ca concentration in the fiber by approximately 1 mM; during the slow time course of the tetanus, most of this Ca is expected to exchange for the equivalent amount of Mg bound in resting frog muscle to the Ca/Mg sites on troponin and parvalbumin.