Several observations indicate that the arterial baroreflex control of sympathetic nerve activity is preserved, even in advanced heart failure. These include: (1) augmentation of muscle sympathetic nerve activity burst amplitude and duration following a premature beat; (2) rapid recognition of changes in blood pressure induced by ventricular arrhythmias; (3) muscle sympathetic alternans and a steep inverse relationship between changes in diastolic pressure and the subsequent sympathetic burst amplitude during pulsus alternans; (4) similar inhibition of muscle sympathetic nerve activity in subjects with normal and impaired left ventricular systolic function by increases in intrathoracic aortic transmural pressure; (5) documentation, by cross-spectral analysis, of similar gain in the transfer function between blood pressure and muscle sympathetic nerve activity in these two groups; and (6) during sodium nitroprusside infusion, similar reflex increases in total body norepinephrine spillover in normal and heart-failure subjects. When nonhypotensive lower-body negative pressure was applied to test the hypothesis that selective reduction of atrial and pulmonary pressures would exert a cardiac sympathoinhibitory response in heart failure, there was no effect in control subjects, but cardiac norepinephrine spillover fell by 25% (P < .05) in those with systolic dysfunction. In summary, human heart failure is characterized by a rapidly responsive and sensitive arterial baroreflex, and by activation of a cardiac sympathoexcitatory reflex related to increased cardiopulmonary filling pressures.