ROLE OF DIETARY MAGNESIUM-DEFICIENCY IN THE PRESSER AND ARRHYTHMOGENIC RESPONSE TO EPINEPHRINE IN THE INTACT DOG

The effect of dietary magnesium deficiency on the presser and arrhythmogenic responses to epinephrine was investigated in 19 dogs maintained either on a normal diet (11 dogs) or a diet deficient in magnesium (8 dogs). Magnesium-deficient dogs had significantly lower serum magnesium levels than the control dogs on a normal diet. Magnesium-deficient dogs showed an increased presser sensitivity to epinephrine as determined by the dose of epinephrine required to cause a maximal presser response (3.4 mu g/kg/min compared to 13.4 mu g/kg/min, p < 0.05). Magnesium-deficient dogs also had a significantly lower threshold dose for ventricular premature beats (0.8 mu g/kg/min compared to 2.7 mu g/kg/min, p < 0.05). Acute administration of magnesium sulfate restored presser sensitivity and ventricular premature beat threshold to normal levels in the magnesium-deficient dogs. Threshold dose for ventricular tachycardia beat was similar in both normal and magnesium-deficient dogs, and threshold was raised significantly in both groups by acute administration of magnesium.