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1 Hypertension Unit, University of Ottawa Heart Institute, Ottawa, ON, Canada
2 Laboratory of Cardiac Growth and Differentiation, Institut de recherches cliniques de Montreal, Montreal, QC, Canada
* To whom correspondence should be addressed. E-mail: fleenen{at}ottawaheart.ca.
In the brain, ouabain-like compounds (OLC) and the renin-angiotensin system (RAS) contribute to sympathetic hyperactivity in rats after myocardial infarction (MI). This study aimed to evaluate changes in components of the central versus peripheral RAS. ACE and AT1 receptor binding densities were determined by measuring 125I-351A and 125I-Ang II binding at 4 and 8 weeks post MI. In the brain, both ACE and AT1 receptors binding increased by 8-15% in the SFO, by 14-22% in the OVLT, by 20-34% in the PVN and by 13-15% in the MnPO. In the heart, ACE and AT1 receptor binding increased the most (nearly 10-fold) in the infarct scar and the least (2-fold) in the right ventricle (RV). In kidneys, both ACE and AT1 receptor binding decreased by 10-15%. After icv infusion of Fab fragments to block brain OLC from 0.5-4 weeks post-MI, increases in ACE and AT1 receptors in the SFO, OVLT, PVN and MnPO were markedly inhibited, and ACE and AT1 receptor densities in the heart increased less (6-fold in the infarct scar). In kidneys, decreases in ACE and AT1 receptor binding were absent after Fab fragments treatment. These results demonstrate that ACE and AT1 receptor binding densities increase not only in the heart but also in relevant areas of the brain of rats post MI. Brain OLC appears to play a major role in the activation of brain RAS in rats post MI, and to a modest degree in the activation of the cardiac RAS.
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