Effects of magnesium supplementation on electrophysiological remodeling of cardiac myocytes in L-NAME induced hypertensive rats

Abstract

Hypertension is one of the major risk factors of cardiac hypertrophy and magnesium deficiency is suggested to be a contributing factor in the progression of this complication. In this study, we aimed to investigate the relationship between intracellular free Mg(2+) levels and electrophysiological changes developed in the myocardium of L-NAME induced hypertensive rats. Hypertension was induced by administration of 40 mg/kg of L-NAME for 6 weeks, while magnesium treated rats fed with a diet supplemented with 1 g/kg of MgO for the same period. L-NAME administration for 6 weeks elicited a significant increase in blood pressure which was corrected with MgO treatment; thereby cardiac hypertrophy developing secondary to hypertension was prevented. Cytosolic free magnesium levels of ventricular myocytes were significantly decreased with hypertension and magnesium administration restored these changes. Hypertension significantly decreased the fractional shortening with slowing of shortening kinetics in left ventricular myocytes whereas magnesium treatment was capable of restoring hypertension-induced contractile dysfunction. Long-term magnesium treatment significantly restored the hypertension-induced prolongation in action potentials of ventricular myocytes and suppressed Ito and Iss currents. In contrast, hypertension dependent decrement in intracellular Mg(2+) level did not cause a significant change in L-type Ca(2+) currents, SR Ca(2+) content and NCX activity. Nevertheless, hypertension mediated increase in superoxide anion, hydrogen peroxide and protein oxidation mitigated with magnesium treatment. In conclusion, magnesium administration improves mechanical abnormalities observed in hypertensive rat ventricular myocytes due to reduced oxidative stress. It is likely that, changes in intracellular magnesium balance may contribute to the pathophysiology of chronic heart diseases.

Dietary intervention reduces left atrial enlargement in dogs with early preclinical myxomatous mitral valve disease: a blinded randomized controlled study in 36 dogs

“…Magnesium (Mg) is a mineral critical for normal cardiac function and provides an antiarrhythmic action [29, 30]. It also reduces hypertension and provides antioxidant and anti-hyperlipidemic effects [31, 32]. In humans, inadequate Mg is correlated with heart failure and increased risk for various cardiovascular disorders [30, 33–35].…”

Correlation of cardiomyocyte apoptosis with duration of hypertension, severity of hypertension and caspase‑3 expression in hypertensive rats

“…Hypertension can cause damage to various target organs in the body (including heart, brain and kidneys) (4). Long-term and sustained hypertension can lead to increased cardiac load, easily resulting in myocardial morphological and structural changes such as cardiac hypertrophy, interstitial fibrosis, ventricular dilatation and cardiomyocyte apoptosis (5). A study has demonstrated that cardiomyocyte apoptosis, as a cytological basis and initiator of left ventricular remodeling of hypertension, plays a regulatory role in the whole ventricular remodeling (6).…”

Low Serum Magnesium as a Predictive Factor of Major Adverse Cardiac and Cerebrovascular Events in Maintenance Hemodialysis Patients

“…Importantly, this study was showed that lower level of magnesium was an independently predictor of MACCE, especially cardiovascular mortality; and serum cTnT concentration was higher in LM group compared with HM group with statistical signi cance. Besides the in uence of vascular damage, in ammation and protein-energy malnutrition by relative magnesium de ciency, magnesium insu ciency was reported to be related to the myocardial remodeling and electrophysiology abnormality [32][33][34].…”