Magnesium and Vascular Tone and Reactivity

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Abstract
It has been reported that the concentration of extracellular magnesium ions ([Mg++]o) can affect blood flow, blood pressure and vascular reactivity in intact mammals. The present studies, using a variety of rat and rabbit blood vessels, were undertaken to shed further light on the relationship between [Mg++]o, Ca++, tone and vascular responsiveness. [Mg++]o was found to differentially affect a variety of hormone and drug-induced contractions in isolated rat and rabbit arteries as well as isolated perfused rat mesenteric arterioles (15–20 µm i.d.). Progressive elevations in [Mg++]o above physiologic levels will dose-dependently produce progressive, increased inhibition of most contractile substances. These results are not reflections of osmolarity. Withdrawal of [Mg++]o can induce contractions of rat arteries as well as of isolated perfused rat mesenteric arterioles. Using isolated rat portal veins, withdrawal of [Mg++] results in rapid enhancement of the spontaneously evoked mechanical responses and increases in rhythmic contractility; these spontaneously evoked responses are abolished in hypermagnesemic solutions (e.g., 10 mM). The contractile responses observed upon withdrawal of [Mg++]o are dependent upon the [Ca++] and the polarity of the membrane but are not related to inhibition of Na+, K+ ATPase. With rat aortic strips, addition of CaEDTA potentiates contractions induced by Mg++ withdrawal, while EGTA promotes rapid relaxations. Rapid relaxations of contractions induced by Mg++ withdrawal in rat aorta could also be induced by Mn++, Ni++, Co++ and Cd++ but not Sr++. Addition of [Ni++] to portal veins exposed either to a Mg++-free solution, or to a solution containing Mg++, results in dose-dependent, and eventual complete, inhibition of all spontaneous mechanical events. These data suggest that [Mg++]o: (a) plays an important role in regulating membrane permeability to [Ca++]o; (b) probably occupies sites which are exchangeable with membrane-bound Ca in arterial, venous and arteriolar smooth muscle; (c) acts intracellularly as well to compete with Ca for certain divalent cation sites; and (d) may play an important role in regulating arteriolar tone and blood pressure.

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