To examine the effects of β-adrenergic blockade on neurohormonal activation in patients with congestive heart failure, 15 men had assessments of hemodynamics and supine peripheral renin and norepmephrine levels before and after 3 months of oral therapy with bucindolol, a nonselective β antagonist. At baseline, plasma renin activity did not correlate with any hemodynamic parameter. However, norepinephrine levels had a weak correlation with left ventricular end-diastolic pressure (r = 0.74, p < 0.01), stroke volume index (r = 0.61, p < 0.02) and pulmonary vascular resistance (r = 0.54, p < 0.05). Plasma renin decreased with bucindolol therapy, from 11.6 ± 13.4 to 4.3 ± 4.1 ng/ml/hour (mean ± standard deviation; p < 0.05), whereas plasma norepinephrine was unchanged, from 403 ± 231 to 408 ± 217 pg/ml. A wide diversity of the norepinephrine response to bucindolol was observed with reduction of levels in some patients and elevation in others. Although plasma norepinephrine did not decrease, heart rate tended to decrease (from 82 ± 20 vs 73 ± 11 min-1, p = 0.059) with β-adrenergic blockade, suggesting neurohormonal antagonism at the receptor level. No changes in I-123 metaiodobenzylguanidine uptake occurred after bucindolol therapy, suggesting unchanged adrenergic uptake of norepinephrine with β-bloker therapy. Despite reductions in plasma renin activity and the presence of β blockade, the response of renin or norepinephrine levels to long-term bucindolol therapy did not predict which patients had improved in hemodynamic status (chi-square = 0.37 for renin, 0.82 for norepinephrine). Thus, β-adrenergic blockade with bucindolol may reduce neurohormonal activation in congestive heart failure, but the reduction in plasma renin activity and norepinephrine may not predict hemodynamk improvement.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine