Contractile and endothelium-dependent dilatory responses of cerebral arteries at various extracellular magnesium concentrations

To clarify the effect of extracellular magnesium (Mg²⁺) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg²⁺ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10^-8-10^-5 M norepinephrine, were significantly potentiated at low Mg²⁺ (0.8 mM v. the normal, 1.2mM). High (1.6 and 2.0 mM) Mg²⁺ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC₅₀ values for norepinephrine were found. The endothelium-dependent relaxations induced by 10^-8-10^-5 M acetylcholine were inhibited by high (1.6 and 2.0 mM) Mg²⁺. Lowering of the Mg²⁺ concentration to 0.8 mM or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC₅₀ values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg²⁺ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg²⁺ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg²⁺ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg²⁺ deficiency in the development of the cerebral vasospasm.