Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 287, Issue 5, Pages H2138-H2146Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00112.2004
Keywords
cardiovascular; neurohumoral; volume regulation; sympathetic activity; forebrain
Funding
- NHLBI NIH HHS [HL-07121, R01 HL-63915] Funding Source: Medline
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Several recent studies suggest an important role for the brain reninangiotensin system in the pathogenesis of heart failure. Angiotensin-converting enzyme ( ACE) activity and binding of angiotensin type 1 (AT(1)) receptors, which mediate the central effects of ANG II, are increased in heart failure. The present study examined the relationship between brain ACE activity and the autonomic dysregulation characteristic of rats with congestive heart failure. Rats with heart failure (HF) induced by coronary artery ligation and sham-operated control ( SHAM) rats were treated with chronic ( 28 days) third cerebral ventricle [intracerebroventricular (ICV)] or intraperitoneal (IP) infusion of a low dose of the ACE inhibitor enalaprilat (ENL) or vehicle (VEH). VEH-treated HF rats had increased sodium consumption, reduced urine sodium and urine volume, and increased sympathetic nerve activity with impaired baroreflex regulation. These responses were minimized or prevented by ICV ENL started 24 h after coronary ligation. IP ENL at the low dose used in these studies had no beneficial effects on HF rats. Neither IP nor ICV ENL had any substantial effect on the SHAM rats. The findings confirm a critically important contribution of the brain renin-angiotensin system to the pathophysiology of congestive heart failure.
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