Why the study?
Does atrial natriuretic peptide improve cardiac and systemic sympathetic responses compared to sodium nitroprusside in patients with congestive heart failure?
Does atrial natriuretic peptide improve cardiac and systemic sympathetic responses compared to sodium nitroprusside in patients with congestive heart failure?
In patients with CHF, ANP does not demonstrate a direct sympathoinhibitory effect compared to SNP, suggesting that vasodilator therapy may only decrease cardiac sympathetic activity if systemic hypotension is avoided.
Neither ANP nor SNP shows direct sympathoinhibition in CHF; hypothesis-generating for BP-dependent effects on cardiac sympathetic activity.
Previous studies have shown that atrial natriuretic peptide (ANP) has relative sympathoinhibitory effects that are of potential benefit in patients with congestive heart failure (CHF). In this study, cardiac and systemic sympathetic responses to ANP were evaluated and compared with responses to sodium nitroprusside (SNP) in patients with CHF. Right- and left-heart hemodynamics were obtained simultaneously with cardiac (CANESP) and total body (TBNESP) norepinephrine spillover; these were measured by using the radiotracer technique. Reductions in arterial blood pressure and cardiac filling pressures were similar with both drugs. ANP and SNP caused a significant and similar increase in TBNESP. Mean values for CANESP did not change in either group, but the response of individual patients was dependent on the effect on diastolic blood pressure (r = -0.71, p<0.01). These results do not provide evidence for a sympathoinhibitory effect of ANP, but suggest that in patients with CHF, cardiac sympathoexcitatory response to arterial baroreceptor unloading may be countered by a potential sympathoinhibitory effect caused by a reduction in cardiac filling pressures. In the setting of CHF, vasodilator therapy may decrease cardiac sympathetic activity if systemic hypotension is avoided.
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Azevêdo et al. (2000) studied this question.
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