Dietary magnesium deficiency increases Giα levels in the rat heart after myocardial infarction

Objective: Magnesium (Mg) is crucial for the function of G proteins which play important roles in mediating the inotropic effects of β adrenergic agonists in the heart and are altered in heart failure. This study was performed to determine whether or not dietary Mg deficiency alters functional activity and levels of the two major ventricular G proteins, Giα and Gsα in the heart after myocardial infarction (MI). Methods: Six week old rats were fed an Mg adequate or deficient diet for 6 weeks. At the end of week 3, MI was induced by coronary artery ligation. A sham operation was performed as control. After surgery, surviving animals were maintained on their assigned diets for another 3 weeks. Then, cardiac function was measured, plasma and tissue were collected. Results: Severe hypomagnesemia and increased plasma catecholamine level were observed in all animals fed the Mg deficient diet. A significant reduction of myocardial Mg concentration accompanied by elevated plasma and myocardial calcium concentrations was observed in MI animals with existing Mg deficiency vs. animals fed the Mg adequate diet. Cardiac function was impaired in MI rats and further reduced in MI rats with existing Mg deficiency. Giα level was not altered by either Mg deficiency or MI alone, but was dramatically elevated in animals with combined Mg deficiency and MI (9.9 ± 0.7 arbitrary unit · mg⁻¹ protein) as compared to MI alone (5.8 ± 0.6, P ` 0.05) and Mg deficiency alone (6.1 ± 0.8, P ` 0.05). Gsα level did not differ between groups. GppNHp-, but not fluoride-stimulated adenylyl cyclase activity was slightly reduced in MI animals with existing Mg deficiency. Conclusion: The findings suggest that dietary Mg deficiency increases the expression of Giα in the heart after MI, while levels and function of Gsα are not compromised during dietary Mg deficiency either with or without MI.