Impaired suppression of plasma norepinephrine during head-down tilt in patients with congestive heart failure

Neurohumoral activation is present in congestive heart failure and may contribute to vasoconstriction in this syndrome. The mechanisms leading to and maintaining neurohumoral activation in long-standing congestive heart failure are as yet undefined. The present study addresses the possibility that baroreceptor-mediated suppression of plasma norepinephrine may be abnormal in patients with long-standing congestive heart failure. Eight normal subjects and 12 patients with long-standing congestive heart failure were studied during 15 minutes of 30 degrees head-down tilt. There were no significant changes in heart rate or arterial blood pressure in either group during these maneuvers. In normal subjects, plasma norepinephrine declined from 257 +/- 38 pg/ml at control to 208 +/- 39 pg/ml during head-down tilt (p less than 0.005). Plasma norepinephrine was elevated in the patients with congestive heart failure, 475 +/- 189 pg/ml, and did not change during head-down tilt. These observations suggest that baroreflex loading maneuvers, which in this study included increased central blood volume and hydrostatic effects on the sinoaortic baroreceptor, do not suppress increased plasma norepinephrine in patients with long-standing congestive heart failure. Impaired baroreflex responsiveness could therefore contribute to either the generation or maintenance of high plasma norepinephrine in this syndrome.