June 1, 2001Annals of the New York Academy of Sciences
The Regulation of Sympathetic Outflow in Heart Failure
Key result
In animal models of chronic heart failure, sympatho-excitation is partly driven by changes in AngII and NO, and chronic exercise training improves depressed baroreflex function and elevated SNA.
Population
Animal models (rabbits) with chronic heart failure (CHF)
Comparison
Modulation of nitric oxide and angiotensin II… vs Non-exercised CHF rabbits, or NO donation alone
Design
Review
Authors
Discussion
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Implication
Challenges baroreflex model of sustained sympatho-excitation in CHF; leaves open humoral mechanisms for targeted study.
Key Points
- This research aims to investigate the role of nitric oxide and angiotensin II in regulating sympathetic outflow in chronic heart failure.
- Examined the effects of nitric oxide and angiotensin II on sympathetic nerve activity in heart failure models.
- Assessed changes in baroreflex function related to exercise training in chronic heart failure rabbits.
- Utilized receptor blockade and NO donation to analyze impacts on sympathetic outflow.
- Chronic exercise training reduced plasma angiotensin II by 20% and sympathetic nerve activity by 25% in CHF rabbits (p<0.05).
- Blockade of AT1 receptors significantly enhanced baroreflex function (HR change ≤ 10% in non-EX CHF rabbits, p<0.01).
- NO donation alone had no effect, suggesting angiotensin II and exercise training are crucial for sympathetic regulation.
Structured PICO
P
Population
Animal models (rabbits) with chronic heart failure (CHF)
I
Intervention
Modulation of nitric oxide (NO) and angiotensin II (AngII) pathways, and chronic exercise training
C
Comparator
Non-exercised CHF rabbits, or NO donation alone
O
Outcome
Sympathetic nerve activity (SNA) and baroreflex functionsurrogate
Preclinical data suggest that sympathetic overactivity in heart failure is mediated by AngII and NO pathways and can be attenuated by chronic exercise training.
Cite This Study
Zucker et al. (2001) conducted a review in Chronic heart failure (CHF). Chronic exercise training vs. No exercise was evaluated. In animal models of chronic heart failure, sympatho-excitation is partly driven by changes in AngII and NO, and chronic exercise training improves depressed baroreflex function and elevated SNA.