Neurohumoral and hemodynamic effects of lower body negative pressure in patients with congestive heart failure

Baroreflex modulation of forearm vascular resistance (FVR) has been reported to be abnormal in patients with congestive heart failure (CHF). However, the neurohumoral mechanisms for this impairment are not defined. We assessed the responses of arterial pressure, FVR, plasma norepinephrine, and plasma renin activity to lower body negative pressure in 29 patients with compensated CHF (New York Heart Association class III and IV) and in 11 normal age-matched control subjects. Baseline mean arterial pressure (83 ± 2 vs 84 ± 2 mm Hg) and mean arterial pressure during LBNP (−10, −20, and −40 mm Hg) were not significantly different in the two groups. Basal FVR (43.7 ± 4 vs 27 ± 2 units), plasma norepinephrine (605 ± 81 vs 155 ± 8 pg/ml), and plasma renin activity (8.3 ± 1.7 vs 1.2 ± 0.2 ng/ml/hr) were significantly ( p < 0.01) higher in patients with CHF. The relative increases in FVR responses during LBNP of −10, −20, and −40 mm Hg (10 ± 4% vs 70 ± 12%, 17 ± 6% vs 106 ± 21%, and 24 ± 9% vs 152 ± 28%) were markedly attenuated in patients with CHF compared to control subjects. Plasma norepinephrine and plasma renin activity responses during LBNP were also attenuated in patients with heart failure. Our results suggest that baroreflex control of FVR and plasma norepinephrine and plasma renin activity is impaired in CHF because of the inability of the cardiopulmonary baroreceptors to alter sympathetic outflow.