The effect of beta -adrenoceptor antagonists (beta -blockers) on neurohormo
nal activation in patients with congestive heart failure has been the subje
ct of study in numerous small clinical trials. Short term therapy with beta
-blockers is associated with a variable acute neurohormonal response which
may be determined by the pharmacology of the agent under study and the bas
eline characteristics of the patient population. Long term therapy with bet
a -blockers devoid of intrinsic sympathomimetic activity (partial agonist a
ctivity) is associated with evidence of decreased plasma markers of activat
ion of the sympathetic nervous system, the renin-angiotensin system, and en
dothelin-1, beta (1)-selective and nonselective beta -blockers appear to be
associated with evidence of decreased neurohormonal activation, with diffe
rential effects on beta -adrenoceptor density. Agents with partial agonist
activity appear to differ from pure antagonists, with some studies reportin
g evidence of increased neurohormonal activation. The mechanisms by which b
eta -blockers reduce neurohormonal activation and the clinical relevance of
changes in adrenergic function to their use in the treatment of heart fail
ure require further investigation.