Background: It has been suggested that a blunted sympathoinhibitory respons
e to atrial natriuretic peptide (ANP) may contribute to the elevation of sy
mpathetic activity seen in heart failure.
Methods and Results: Experiments were performed in anesthetized rats 6 to 9
weeks after coronary ligation to induce heart failure. Responses to intrav
enous injections of ANP (4 mu g/kg) did not differ between the sham-operate
d (n = 11) and heart-failure (n = 7) rats. Before sinoaortic denervation. A
NP decreased mean arterial pressure (MAP) by 8 mm Hg in both the heart-fail
ure and sham rats, renal sympathetic nerve activity (RSNA) by 9% to 10% in
both groups, and heart rate (HR) by 12 to 13 beats/min in both groups. Afte
r baroreceptor denervation, ANP decreased MAP by approximately 22 mm Hg, RS
NA by 14%, and HR by 16 beats/min in both the heart-failure and sham rats.
After vagotomy, there was no longer a significant decrease in RSNA or HR in
response to ANP.
Conclusion: The sympathoinhibitory effects of ANP are maintained in heart f
ailure. This suggests that the elevated sympathetic activity observed in he
art failure cannot be attributed to a blunting of the response to ANP.