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Articles in PresS, published online ahead of print April 18, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00032.2002
Submitted on January 16, 2002
Accepted on April 11, 2002
1 Biology, Queen's University, Kingston, Ontario, Canada
2 Pharmacology, Queen's University, Kingston, Ontario, Canada
* To whom correspondence should be addressed. E-mail: moyesc{at}biology.queensu.ca.
The present study used spontaneously hypertensive rats to investigate the remodeling of cardiac bioenergetics associated with changes in blood pressure. Blood pressure was manipulated using an aggressive anti-hypertensive treatment combining low dietary salt and the angiotensin-converting enzyme inhibitor enalapril. Successive cycles of 2 weeks on treatment, 2 weeks off treatment led to rapid, reversible changes in left ventricular mass (30% change in <10d). Despite changes in left ventricular mass, the specific activities of bioenergetic (COX, CS, LDH) and ROS (total cellular SOD) enzymes were actively maintained within relatively narrow ranges regardless of the treatment duration, organismal age or transmural region. Although enalapril treatment led to parallel declines in mitochondrial enzyme content and ventricular mass, total ventricular mtDNA content was unaffected. Altered enzymatic content occurred without significant changes in relevant mRNA and protein levels. Transcript levels of gene products involved in mtDNA maintenance (Tfam), mitochondrial protein degradation (LON protease), fusion (fuzzy onion homologue) and fission (dynamin-like protein, synaptojanin-2
) were also unchanged. In contrast, enalapril-mediated ventricular and mitochondrial remodeling was accompanied by a 2-fold increase in the specific activity of catalase, a sensitive indicator of oxidative stress. This suggests that rapid cardiac adaptation is accompanied by the tight regulation of mitochondrial enzyme activities, as well as increased ROS production.
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