One of the hallmarks of chronic congestive heart failure is an increase in 
sympathetic tone to the peripheral circulation and to the heart. A correlation 
between plasma norepinephrine and the severity of the heart failure state has 
been demonstrated. One mechanism that has been proposed to account for this 
sympathoexcitation is a depression in the baroreflex and, perhaps, cardiac 
reflex control of sympathetic nerve activity. This review summarizes work from 
several laboratories, including our own, that documents a depressed baroreflex 
control of heart rate and sympathetic nerve activity in both animals and humans 
with heart failure. The mechanism of the depressed baroreflex most likely is 
caused by reduced baroreceptor sensitivity as well as enhanced input to the 
central nervous system from cardiac receptors that are chemosensitive. Although 
sympathetic tone and arterial baroreflex sensitivity are altered in heart 
failure, there have been no studies showing a cause-and-effect relationship. 
Increases in plasma norepinephrine are similar in baroreceptor-denervated and 
intact dogs paced into heart failure. This latter observation cells into 
question the traditional concept of baroreceptor-mediated increases in 
sympathetic tone in heart failure.