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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

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Sarcoplasmic reticulum Ca2+ transport and gene expression in congestive heart failure are modified by imidapril

Qiming Shao1, Bin Ren, Harjot K Saini

  • 1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, 351 Tache Ave., Winnipeg, Manitoba, Canada R2H 2A6.

American Journal of Physiology. Heart and Circulatory Physiology
|December 4, 2004
PubMed

Insights

Blocking the renin-angiotensin system with imidapril improves heart function in congestive heart failure by preserving sarcoplasmic reticulum protein gene expression and function.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pharmacology

Background:

  • Congestive heart failure (CHF) involves impaired cardiac function due to altered sarcoplasmic reticulum (SR) protein gene expression.
  • Myocardial infarction (MI) is a common cause of CHF, leading to significant cardiac dysfunction.

Purpose of the Study:

  • To investigate if blocking the renin-angiotensin system (RAS) improves cardiac function in CHF by preventing changes in SR protein gene expression.
  • To examine the effects of imidapril, an angiotensin-converting enzyme (ACE) inhibitor, on SR Ca(2+) transport and protein expression in rats with MI.

Main Methods:

  • Rats with induced MI were treated with imidapril (1 mg/kg/day) for 4 weeks.
  • Assessed cardiac function, SR Ca(2+) uptake and release activities, and protein/mRNA levels of key SR proteins (Ca(2+) pump ATPase, phospholamban, ryanodine receptor).

Main Results:

  • Imidapril treatment improved cardiac performance in infarcted rats.
  • It prevented the decrease in SR Ca(2+) transport, pump, and release activities.
  • Imidapril also preserved the protein content and mRNA levels of SR proteins, which were reduced in untreated failing hearts.

Conclusions:

  • Blockade of the RAS, demonstrated by imidapril, improves cardiac function in CHF post-MI.
  • This improvement is linked to the prevention of altered SR protein gene expression and maintenance of SR Ca(2+) transport.
  • ACE inhibitors and ANG II receptor antagonists show similar beneficial effects, supporting RAS blockade as a therapeutic strategy.

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