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Central Ang‐(1–7) enhances baroreflex gain in rabbits with chronic heart failure
Author(s) -
Kar Sumit,
Curry Pamela L,
Zucker Irving H
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.625.4
Subject(s) - baroreflex , heart failure , angiotensin ii , medicine , renin–angiotensin system , heart rate , endocrinology , blood pressure , anesthesia , cardiology
In chronic heart failure (CHF), arterial baroreflex function is impaired in part by activation of the central renin‐angiotensin system. A metabolite of Angiotensin II (Ang II), Ang‐(1–7), has been shown to exhibit cardiovascular effects that are in opposition to that of Ang II. However, the action of Ang‐(1–7) on sympathetic outflow and baroreflex function is not well understood, especially in CHF. This study aimed to determine the effect of intracerebroventricular infusion of Ang‐(1–7) on baroreflex control of heart rate (HR) in rabbits with CHF. We hypothesized that central Ang‐(1–7) would improve baroreflex function in CHF. Ang‐(1–7) (2 nmol/μl/hour) or artificial cerebrospinal fluid (1 μl/hour) was infused by an osmotic mini‐pump for 4 days in sham and pacing‐induced CHF rabbits (n=5–6/group). CHF rabbits showed depressed baroreflex gain in the conscious state. Ang‐(1–7) treatment increased baroreflex gain (7.4±1.5 bpm/mm Hg vs. 2.5±0.4 bpm/mm Hg, P<.05). Central Ang‐(1–7) improved baroreflex control in CHF by lowering minimum HR and increasing maximum gain. This suggests that modulation of baroreflex function by Ang‐(1–7) may be due to increased vagal tone. Source of support: PO1 HL‐62222