Regulation of Sympathetic Nerve Activity in Heart Failure
Key result
In rabbits with chronic heart failure, combined angiotensin II receptor blockade and exogenous nitric oxide reduced renal sympathetic nerve activity to 65.2% of control levels (P<0.0001).
Population
24 New Zealand White rabbits, including a pacing-induced chronic heart failure model and normal controls.
Comparison
1-hour infusion of sodium nitroprusside after… vs Normal rabbits undergoing the same protocol, and…
Design
Preclinical
Authors
Discussion
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Implication
May inform sympathetic modulation strategies in heart failure; leaves open clinical translation pending human studies.
Structured PICO
P
Population
24 New Zealand White rabbits, including a pacing-induced chronic heart failure (CHF) model (paced at 360 to 380 bpm for ~3 weeks) and normal controls.
I
Intervention
1-hour infusion of sodium nitroprusside (SNP; 3 microgram . kg-1. min-1) after Ang II blockade with losartan (5 mg/kg), with mean arterial pressure readjusted using phenylephrine.
C
Comparator
Normal rabbits undergoing the same protocol, and baseline measurements before losartan.
O
Outcome
Changes in renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP).surrogate
Main Result
p-value: p=<0.0001
In a rabbit model of heart failure, both a loss of nitric oxide and an increase in angiotensin II are necessary for sustained increases in sympathetic nerve activity.
Cite This Study
Liu et al. (1999) studied Chronic heart failure (n=24). Sodium nitroprusside (SNP) and losartan vs. Normal rabbits and baseline was evaluated on Renal sympathetic nerve activity (RSNA) (p=<0.0001). In rabbits with chronic heart failure, combined angiotensin II receptor blockade and exogenous nitric oxide reduced renal sympathetic nerve activity to 65.2% of control levels (P<0.0001).