Three experiments were conducted examining the contribution of beta-ad
renergic receptors to stress-induced cholesterol increases. Rats were
exposed to 3 90-min sessions of inescapable tailshock, or left undistu
rbed in their home cage. Propranolol, a nonselective beta-blocker, att
enuated the stress-induced cholesterol increase when administered prio
r to the daily shack session. Atenolol, a beta-1 specific antagonist,
also attenuated the stress-induced cholesterol increase. Butoxamine, a
beta-2 specific antagonist, had no effect on the stress-induced chole
sterol increases. Results are discussed in terms of catecholamine-stim
ulated free fatty acid (FFA) release as a potential mechanism for prod
ucing stress-induced hypercholesterolemia. Copyright (C) 1996 Elsevier
Science Inc.