Perfused rat hearts release or accumulate approximately 10% of total Mg2+ content when stimulated with norepinephrine (NE) or carbachol, respectively. Collagenase-dispersed rat ventricular myocytes increase or decrease total cell Mg2+ by 1 mM within 5 minutes when stimulated with these same transmitters. Measurements of Mg2+ transport using 28Mg or atomic absorbance spectrophotometry indicate that the rate and the extent of both stimulated Mg2+ efflux and influx are independent of the concentration of extracellular Mg2+ (0 to 1.2 mM). Mg2+ release induced by NE is rapidly reversed by the addition of carbachol, and Mg2+ uptake induced by carbachol is reversed by NE. Decreasing extracellular Na+ or Ca2+ decreases or abolishes Mg2+ efflux from myocytes. Cd2+ or other Ca2+ channel blockers also inhibit Mg2+ efflux in the presence of a physiological concentration of extracellular Ca2+. Replacement of extracellular Ca2+ with Sr2+ or with Mn2+ decreases or abolishes both stimulated efflux and influx of Mg2+. Redistribution of 85Sr in myocytes and in the supernatant indicates that under those conditions Sr2+ is released or accumulated by NE or carbachol in a manner similar to that of Mg2+. Hence, at least in the case of Sr2+, the inhibition of Mg2+ fluxes can be explained by the transport of Sr2+ rather than Mg2+ through the transport(s) systems. By contrast, replacement of extracellular Ca2+ with Ba2+ inhibits stimulated Mg2+ uptake but not Mg2+ release. These results indicate that cardiac myocytes have a major pool of Mg2+ that can be rapidly mobilized upon hormonal stimulation. The net uptake and release of Mg2+ are quantitatively similar and appear to be independent of the extracellular Mg2+ concentrations but are affected, to various degrees, by the presence of other cellular or extracellular cations.

A large Mg:* cell uptake against concentration gradients is stimulated in collagenase-disper~ed ra: myocytes by carbachol and in hepato~t~ by carbachol or vasoprcssin. The signalling pathway(s) responsible for this stimulation o1" Mg ~-+ uptake was inv.+stigated by using various activators or inhibitors of protein kinase C (PKC) and by correlatin/~ Mg :+ uptake with cell PKC activity and cAMP content. In both cell preparations, the dir~.,ct stimulation of PKC by diaeylglycerol analogs or phorbol esters reproduce the same pattern of MS -+" uptake as that induced by carbachol or vasopressin. These data indicate that the activation of PKC is responsible for a stimulation of Mg:" uptake by myocytes or hepatocytes, whereas increase in cAMP in these cells stimulates Mg a' release.

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