Impaired baroreceptor control of renal sympathetic activity in human chronic heart failure

The regulation of renal sympathetic activity in the setting of heart failure is largely unexplored. We used the norepinephrine spillover method to address the hypothesis that baroreflex control of renal sympathetic activity is blunted in heart failure.

Twenty-two patients were studied, 11 in a group with heart failure and 11 in a group with normal ventricular function. In both groups, renal norepinephrine spillover was assessed in response to sodium nitroprusside infused to steady-state conditions. Sodium nitroprusside resulted in significant reductions in mean systemic arterial pressure (normal group, -13+/-1% [mean+/-SEM]; heart failure group, -12+/-1%). In response to nitroprusside, there was an 85+/-34% increase in renal norepinephrine spillover in the normal group (from 537+/-84 to 840+/-140 pmol/min, P<0.05). Despite similar hemodynamic responses to nitroprusside in the heart failure group, renal norepinephrine spillover was unchanged (from 1420+/-153 to 1387+/-161 pmol/min, P=NS), a response that was significantly different from that seen in the normal group.

In patients with heart failure, compared with those with normal ventricular function, renal sympathetic activity did not change in response to a steady-state infusion of sodium nitroprusside. This result provides evidence for reduced baroreflex control of renal sympathetic activity in heart failure.