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- Title
Both enalapril and losartan attenuate sarcolemmal Na<sup>+</sup>-K<sup>+</sup>-ATPase remodeling in failing rat heart due to myocardial infarction.
- Authors
Xiaobing Guo; Jingwei Wang; Elimban, Vijayan; Dhalla, Naranjan S.
- Abstract
To investigate the mechanisms underlying the depressed sarcolemmal (SL) Na+-K+-ATPase activity in congestive heart failure (CHF), different isoforms and gene expression of Na+-K+-ATPase were examined in the failing left ventricle (LV) at 8 weeks after myocardial infarction (MI). In view of the increased activity of renin-angiotensin system (RAS) in CHF, these parameters were also studied after 5 weeks of treatment with enalapril (10 mg·kg-1·day-1), an angiotensin-converting enzyme inhibitor, and losartan (20 mg·kg-1·day-1), an angiotensin II type 1 receptor antagonist, starting at 3 weeks after the coronary ligation in rats. The infarcted animals showed LV dysfunction and depressed SL Na+-K+-ATPase activity. Protein content and mRNA levels for Na+-K+-ATPase α2 isoform were decreased whereas those for Na+-K+-ATPase α3 isoform were increased in the failing LV. On the other hand, no significant changes were observed in protein content or mRNA levels for Na+-K+-ATPase α1 and β1 isoforms. The treatment of infarcted animals with enalapril or losartan improved LV function and attenuated the depression in Na+-K+-ATPase α2 isoform as well as the increase in α3 isoform, at both the protein and mRNA levels; however, combination therapy with enalapril and losartan did not produce any additive effects. These results provide further evidence that CHF due to MI is associated with remodeling of SL membrane and suggest that the blockade of RAS plays an important role in preventing these alterations in the failing heart.
- Subjects
ADENOSINE triphosphatase; HEART diseases; THERAPEUTICS; MYOCARDIAL infarction; ANGIOTENSINS; HEART ventricles; BLOOD circulation disorders
- Publication
Canadian Journal of Physiology & Pharmacology, 2008, Vol 86, Issue 4, p139
- ISSN
0008-4212
- Publication type
Article
- DOI
10.1139/Y08-006