Magnesium plays an important role in neurochemical transmission and muscular excitability.
The mechanism of action of magnesium sulfate is not as well described but is thought to
competitively block intracellular calcium channels, decreasing calcium availability and thus
inhibiting smooth muscle contractility (i.e. causes vasodilation, Slows SA node impulse
formation and prolongs conduction time). The drug is thus contraindicated in patients with
heart block or myocardial damage.
It also competes with calcium at the motor end plate, where it reduces excitation by inhibiting acetyl choline release and ultimately causing skeletal muscle relaxation (thus used to prevent or control convulsions). Because . . .
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