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1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Departments of Physiology, Faculty of Medicine; 2Human Nutritional Sciences, Faculty of Human Ecology, University of Manitoba, Winnipeg, Canada; and 3Aoto Hospital, Department of Internal Medicine, Jikei University, Tokyo, Japan
Submitted 28 December 2004 ; accepted in final form 27 January 2005
The activities of both sarcolemmal (SL) Na+-K+-ATPase and Na+/Ca2+ exchanger, which maintain the intracellular cation homeostasis, have been shown to be depressed in heart failure due to myocardial infarction (MI). Because the renin-angiotensin system (RAS) is activated in heart failure, this study tested the hypothesis that attenuation of cardiac SL changes in congestive heart failure (CHF) by angiotensin-converting enzyme (ACE) inhibitors is associated with prevention of alterations in gene expression for SL Na+-K+-ATPase and Na+/Ca2+ exchanger. CHF in rats due to MI was induced by occluding the coronary artery, and 3 wk later the animals were treated with an ACE inhibitor, imidapril (1 mg·kg–1·day–1), for 4 wk. Heart dysfunction and cardiac hypertrophy in the infarcted animals were associated with depressed SL Na+-K+-ATPase and Na+/Ca2+ exchange activities. Protein content and mRNA levels for Na+/Ca2+ exchanger as well as Na+-K+-ATPase 
1-, 2- and 
1-isoforms were depressed, whereas those for 3-isoform were increased in the failing heart. These changes in SL activities, protein content, and gene expression were attenuated by treating the infarcted animals with imidapril. The beneficial effects of imidapril treatment on heart function and cardiac hypertrophy as well as SL Na+-K+-ATPase and Na+/Ca2+ exchange activities in the infarcted animals were simulated by enalapril, an ACE inhibitor, and losartan, an angiotensin receptor antagonist. These results suggest that blockade of RAS in CHF improves SL Na+-K+-ATPase and Na+/Ca2+ exchange activities in the failing heart by preventing changes in gene expression for SL proteins.
cardiac sarcolemma; Na+-K+-ATPase isoforms; cardiac gene expression; congestive heart failure; angiotensin-converting enzyme inhibitors
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