Intra-arterial ANP administration increased forearm vascular volume similarly in heart failure patients and controls (14.7% vs 13.4%), while the arterial blood flow response was blunted (P<0.01).
Do exogenous and endogenous natriuretic peptides have preserved venodilator and arterial effects in patients with chronic heart failure compared to controls?
In chronic heart failure, venous responsiveness to ANP is preserved despite arterial resistance, suggesting arterial endothelial dysfunction contributes to natriuretic peptide resistance.
Tasa de eventos absoluta: 14.7% vs 13.4%
OBJECTIVE: Natriuretic peptides (NPs) reduce central venous pressure in patients with chronic heart failure (cHF) despite attenuation of arterial, renal, and humoral effects. This suggests a preserved venodilator response. This study had 4 aims: to compare the venodilator effects of human NPs in patients with cHF; to assess the contribution of basal ANP and BNP levels to regulation of forearm vascular volume (FVV); to test the hypothesis that venous ANP responsiveness is preserved in cHF; and to assess the involvement of endothelial nitric oxide-synthase (eNOS) in NP-induced vascular effects. METHODS AND RESULTS: Venous and arterial forearm vascular responses to incremental intra-arterial doses of ANP, Urodilatin, BNP, CNP, or the ANP receptor antagonist A71915 were studied in 53 patients and 11 controls. ANP receptor antagonism reduced FVV by 4.4%+/-1.2% (P<0.05). The forearm blood flow (FBF) response to ANP was significantly blunted in patients versus controls (P<0.01), whereas FVV increased similarly in both groups (maximum 14.7% and 13.4%, both P<0.001). The eNOS blockade reduced ANP-induced FBF changes in controls but not in patients (P<0.05), whereas similar reductions in FVV changes were seen in groups (both P<0.001). CONCLUSIONS: In cHF venous, but not arterial, ANP responsiveness is preserved. Arterial endothelial dysfunction may contribute to NP resistance.
Schmitt et al. (Tue,) conducted a other in chronic heart failure (n=64). Natriuretic peptides (ANP, Urodilatin, BNP, CNP) and ANP receptor antagonist A71915 vs. controls was evaluated on Maximum forearm vascular volume (FVV) increase in response to ANP. Intra-arterial ANP administration increased forearm vascular volume similarly in heart failure patients and controls (14.7% vs 13.4%), while the arterial blood flow response was blunted (P<0.01).