title: 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.
authors.affiliation: Faculty of Medicine, Department of Biophysics, Akdeniz University, Antalya, Turkey.
authors.forename: Nihal
authors.initials: N
authors.lastname: Ozturk
authors.affiliation: Faculty of Medicine, Department of Biophysics, Akdeniz University, Antalya, Turkey.
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Olgar
authors.affiliation: Faculty of Medicine, Department of Biochemistry, Akdeniz University, Antalya, Turkey.
authors.forename: Mutay
authors.initials: M
authors.lastname: Aslan
authors.affiliation: Faculty of Medicine, Department of Biophysics, Akdeniz University, Antalya, Turkey. osemir@akdeniz.edu.tr.
authors.forename: Semir
authors.initials: S
authors.lastname: Ozdemir
mesh_terms: D000818:Animals; D064752:Atrial Remodeling / Q000187:drug effects*; D002118:Calcium / Q000378:metabolism; D006332:Cardiomegaly / Q000517:prevention & control; D019587:Dietary Supplements; D006352:Heart Ventricles / Q000473:pathology; D006973:Hypertension / Q000139:chemically induced*; D008274:Magnesium / Q000008:administration & dosage / Q000494:pharmacology*; D032383:Myocytes, Cardiac / Q000473:pathology*; D019331:NG-Nitroarginine Methyl Ester; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats
chemical_list: D008274:Magnesium; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester
keywords: Excitation-contraction coupling; Heart; Hypertension; L-NAME; Mg2+; ROS