Effect of Atorvastatin on Activity of Myocardial Sarcoplasmic Reticulum Calcium Pump in Pressure-loaded Hypertensive Rats
Wang Nian-don
Abstract
Wang Nian-don
Abstract
Objective To investigate the effect of atorvastatin on left ventricular hypertrophy induced by pressure overload and the activity of myocardial sarcoplasmic reticulum calcium(SERCA).Methods Left ventricular hypertrophy was induced by abdominal aortic constriction(AAC) in adult SD rats, and received atorvastatin 10 mg/(kg·d)(n=10), atorvastatin 30 mg/(kg·d)(n=10), amlodipine group(5 mg/kg·d)(n=10).Sham operated rats(n=10) and untreated AAC rats(n=10) served as controls.Systolic blood pressure (SBP) and LVMI were determined, cardiomyocytes diameter were measured by HE stain; the activity of myocardial SERCA was determined by non-polar phosphate method; Ca2+ concentration in cardiomyocytes was detected by dual wave spectrofluorometer.ResultsCompared with sham operation group, SBP, LVMI, mean diameter of cardiomyocytes and Ca2+ concentration of cardiomyocytes in AAC rats were significantly increased; while the activity of myocardium SERCA (4.0±0.6) vs (6.4±0.8) μmol/(mg pro·h) was significantly decreased (all P0.05).SBP, LVMI, mean diameter of cardiomyocytes and Ca2+ concentration of cardiomyocytes in AAC rats were significantly decreased in both atorvastatin 30 mg/(kg·d) and amlodipine group. The activity of myocardium SERCA [Ato 30 mg (4.9±0.4), amlodipine (4.8±0.5) vs AAC(4.0±0.6) μmol/(mg pro·h), all P0.05] was significantly increased in atorvastatin and amlodipine treated groups.ConclusionHigh dose of atorvastatin could prevent AAC induced left ventricular hypertrophy, possibly via increaing the activity of myocardial SERCA and reducing Ca2+ concentration in hypertrophic myocardial cells.
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Objective To investigate the effect of atorvastatin on left ventricular hypertrophy induced by pressure overload and the activity of myocardial sarcoplasmic reticulum calcium(SERCA).Methods Left ventricular hypertrophy was induced by abdominal aortic constriction(AAC) in adult SD rats, and received atorvastatin 10 mg/(kg·d)(n=10), atorvastatin 30 mg/(kg·d)(n=10), amlodipine group(5 mg/kg·d)(n=10).Sham operated rats(n=10) and untreated AAC rats(n=10) served as controls.Systolic blood pressure (SBP) and LVMI were determined, cardiomyocytes diameter were measured by HE stain; the activity of myocardial SERCA was determined by non-polar phosphate method; Ca2+ concentration in cardiomyocytes was detected by dual wave spectrofluorometer.ResultsCompared with sham operation group, SBP, LVMI, mean diameter of cardiomyocytes and Ca2+ concentration of cardiomyocytes in AAC rats were significantly increased; while the activity of myocardium SERCA (4.0±0.6) vs (6.4±0.8) μmol/(mg pro·h) was significantly decreased (all P0.05).SBP, LVMI, mean diameter of cardiomyocytes and Ca2+ concentration of cardiomyocytes in AAC rats were significantly decreased in both atorvastatin 30 mg/(kg·d) and amlodipine group. The activity of myocardium SERCA [Ato 30 mg (4.9±0.4), amlodipine (4.8±0.5) vs AAC(4.0±0.6) μmol/(mg pro·h), all P0.05] was significantly increased in atorvastatin and amlodipine treated groups.ConclusionHigh dose of atorvastatin could prevent AAC induced left ventricular hypertrophy, possibly via increaing the activity of myocardial SERCA and reducing Ca2+ concentration in hypertrophic myocardial cells.
Key concepts: Amlodipine, SERCA, Internal medicine, Atorvastatin, Left ventricular hypertrophy, Medicine, Endocrinology, Pressure overload