Magnesium as the physiologic calcium antagonist: its vascular effects and therapeutic use

Summary

Clinical studies have demonstrated that the unstable or primary angina attacks are caused by severe spastic occlusion of morphologically healthy or partially sclerotic segments of coronary vessels. The suggestion, expressed by some authors, that these spasms may be induced by hypomagnesemia is controversial. The present in-vitro experiments, carried out in isolated strips of coronary vessels (dogs and pigs) and other peripheral blood vessels (bovine facial arteries and veins) do not contradict the conclusion that the increase in basal tone observed after treatment of the vessel preparations with magnesium-free physiologic solutions may possibly represent one triggering factor for the induction of vasospasms, but they favour the concept that these spasms are primarily due to rhythmic contractions initiated by potential pacemaker cells occurring in the wall of the coronary vessels after degenerative processes. They show furthermore that an elevation of Mg_o (from 0.5 to 10 mmol/1) can reduce significantly the basal, physiologic tone as well as the tone resulting from an increased transmembrane Ca-ion movement taking place during membrane depolarization or after receptor stimulation. Since magnesium probably represents the most adequate blocker of calcium fluxes, there seems to be no argument against its prophylactic and therapeutic use.