Resting hemodynamic measurements and plasma levels of catecholamines and renin activity were studied in 55 hospitalized treated patients with congestive heart failure in clinically stable condition. Plasma norepinephrine (mean ± standard error of the mean 594 ± 51 pg/ml, range 153 to 1,868) and plasma renin activity (mean 12.9 ± 2.4 ng/ml per hr, range 0.6 to 85.2) values were significantly (probability [p] < 0.01) higher than in normal subjects. In 26 of these patients plasma norepinephrine and plasma renin activity measured on 3 successive days including the day of hemodynamic study did not change significantly. In contrast, plasma epinephrine (mean 138 ± 26 pg ml, range 24 to 1,099) increased significantly at the time of invasive studies, probably because of stress-induced adrenal discharge. When baseline plasma norepinephrine was compared with resting hemodynamic values, significant correlations were found with right atrial pressure (correlation coefficient [r] = +0.44), pulmonary arterial pressure (r = +0.45), pulmonary capillary wedge pressure (r = +0.42), pulmonary vascular resistance (r = +0.55), pulmonary arteriolar resistance (r = +0.41), cardiac index (r = -0.42), systemic vascular resistance (r = +0.30) and heart rate (r = +0.52). Plasma renin activity was only weakly correlated with plasma norepinephrine (r = +0.38) and did not correlate significantly with any hemodynamic measurement. It is concluded that patients with congestive heart failure can be categorized on the basis of neurohumoral activity. The statistically significant correlations between plasma norepinephrine and hemodynamic evidence of cardiac dysfunction suggest that the sympathetic response is either a marker of or a contributor to the hemodynamic derangement. Because hemodynamic abnormalities did not correlate with plasma renin activity despite a statistically significant correlation between plasma norepinephrine and plasma renin activity, it appears that the two systems are independently activated in congestive heart failure but that sympathetic stimulation may be one factor contributing to renin release. Further studies are needed to assess the usefulness of plasma hormone levels in evaluating and treating patients with congestive heart failure.