Influence of altering cellular magnesium content on vascular smooth muscle contractility

Tissue and cellular Mg levels in porcine carotid arterial strips were varied by 4-h incubation in high-K+, Ca2+-free solutions containing variable amounts of MgCl2 (0, 0.6, 1.2, 3, 5, 10, and 15 mM). The total Mg content, designated tissue Mg, was determined immediately after the incubation and also 1 and 3 h after reexposure to a normal physiological salt solution (PSS) containing 1.2 mM Mg2+. Cellular Mg levels were calculated from this data. The tissue Mg was profoundly altered immediately following the incubation, with values ranging from 7.3 mumol/g dry wt to 71.4 mumol/g dry wt, but remained significantly elevated following reexposure to normal PSS only in those strips incubated in 15 mM Mg2+. The calculated cellular Mg levels, however, did remain significantly elevated if 1 microM ouabain was included in both the incubation and post-incubation solutions. The response to high K+ in tissues subjected to the same 4-h incubation procedure exhibited the same pattern as the cellular Mg levels. Postincubation changes in the response to norepinephrine, either in the presence or absence of external Ca2+, depended on both the dose of norepinephrine and the level of Mg2+ in the incubation medium. It appears sarcoplasmic Mg levels are capable of modulating arterial contractility through influences at both the level of contractile proteins and the delivery of activator Ca2+.