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Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes

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Regulation of phospholamban and sarcoplasmic reticulum Ca2+-ATPase by atorvastatin: implication for cardiac

Lan Kang¹, Qiang Fang, Shen-Jiang Hu

¹Institute of Cardiology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, PR China.

Archives of Pharmacal Research

|July 10, 2007

Insights

Atorvastatin, a statin, prevents cardiac hypertrophy in spontaneously hypertensive rats by improving intracellular calcium handling. It normalizes sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) levels and activity, reducing heart size and blood pressure.

Area of Science:

Cardiovascular Biology
Molecular Cardiology
Pharmacology

Background:

Abnormal intracellular calcium (Ca2+) homeostasis is implicated in cardiac hypertrophy.
HMG-CoA reductase inhibitors (statins) may prevent this process.
The specific mechanisms of statins in cardiac hypertrophy require further elucidation.

Purpose of the Study:

To investigate the effect of atorvastatin on left ventricular hypertrophy in spontaneously hypertensive rats (SHR).
To explore the underlying mechanism involving intracellular Ca2+ homeostasis, specifically phospholamban (PLB) and sarcoplasmic reticulum Ca2+-ATPase (SERCA2a).

Main Methods:

Used spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) over ten weeks.
Administered atorvastatin or distilled water.
Analyzed mRNA and protein expression of PLB and SERCA2a using RT-PCR and Western blotting.
Assessed SERCA2a activity via a colorimetric method.
Measured cardiac hypertrophic indices, systolic blood pressure (SBP), and serum lipids.

Main Results:

SHR hearts showed decreased SERCA2a mRNA, protein, and activity, indicative of impaired Ca2+ handling.
Atorvastatin treatment significantly inhibited these decreases in SHR.
Atorvastatin reduced cardiac hypertrophy indices, SBP, and serum lipids in SHR.
No significant changes in PLB expression were observed across groups.

Conclusions:

Atorvastatin prevents cardiac hypertrophy in SHR, likely by regulating SERCA2a levels and activity.
This regulation of intracellular Ca2+ homeostasis offers a novel insight into atorvastatin's cardioprotective effects.
Findings suggest atorvastatin's potential in managing pressure overload-induced cardiac hypertrophy.

Read full analysis

Abstract:

Abnormal intracellular Ca2+ homeostasis in the myocardium has been suggested as the cause of cardiac hypertrophy, and this process can be prevented by the HMG-CoA reductase inhibitors, statins. In the present study, the effect of atorvastatin on left ventricular hypertrophy was investigated, and then whether the underlying mechanism was related to a defect in intracellular Ca2+ homeostasis explored. Twelve spontaneously hypertensive rats (SHR), at 8 weeks old, were used in this study, and received either distilled water or atorvastatin for ten weeks, with age-matched normotensive Wistar-Kyoto rats (WKY) used as controls. RT-PCR and western blotting were used to detect the mRNA and protein expressions of phospholamban (PLB) and sarcoplasmic reticulum Ca2+-ATPase (SERCA2a), respectively, and a colorimetric method used to examine the SERCA2a activity. Additionally, cardiac hypertrophic indices, such as the cardiosomatic ratio, left ventricular weight to body weight (LVW/BW) ratio and cardiomyocytes transverse diameter (TDM), together with the systolic blood pressure (SBP) and serum lipids levels were also examined. After ten weeks, significant decreases were observed in both the mRNA and protein expression levels of SERCA2a, as well as its activity, in the hypertrophied hearts of the SHR. The administration of atorvastatin to the same strains of rats effectively inhibited these decreases, and the above cardiac hypertrophic indices, as well as the SBP and serum lipids levels were significantly decreased. However, no significant changes in the expressions of PLB were observed in WKY, SHR and atorvastatin-treated SHR. These findings demonstrated that through regulation of the PLB and SERCA2a levels in the hearts of SHR, atorvastatin can prevent the cardiac hypertrophy caused due to pressure overload, which provides a relatively new insight into the mechanism of atorvastatin in the prevention of cardiac hypertrophy.

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