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Magnesium affects excitation, conduction, and contraction of isolated mammalian cardiac muscle.

An increase of extracellular Mg concentration, [Mg]o, reduced myocardial excitability and conduction without affecting the resting membrane potential or action potential configuration in ventricular myocytes and papillary muscles from a number of mammalian species. Although there was a small increase of specific membrane resistance and no change to intracellular resistivity, the threshold voltage was shifted to depolarized potentials. Thus loss of excitability can be explained by a shift of the activation of inward currents to depolarized potentials, and reduced conduction velocity is due solely to a diminution of local circuit currents. Mgo also was negatively inotropic, the magnitude of this effect being species dependent. Raised [Mg]o caused a small increase of intracellular [Mg] with a small decrease of intracellular [Na+], did not affect intracellular pH, and attenuated the intracellular Ca2+ transient associated with cell shortening in rat (but not rabbit) myocytes. An increase of [Mg]o reduced the magnitude of the voltage-dependent inward Ca2+ current, ICa, in rat and rabbit myocytes, and the activation curve of ICa was shifted to more depolarized potentials. A scheme to account for the negative inotropic effect of Mg is presented.