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Three experiments were conducted examining the contribution of β-adrenergic receptors to stress-induced cholesterol increases. Rats were exposed to 3 90-min sessions of inescapable tailshock, or left undisturbed in their home cage. Propranolol, a nonselective β-blocker, attenuated the stress-induced cholesterol increase when administered prior to the daily shock session. Atenolol, a β-1 specific antagonist, also attenuated the stress-induced cholesterol increase. Butoxamine, a β-2 specific antagonist, had no effect on the stress-induced cholesterol increases. Results are discussed in terms of catecholamine-stimulated free fatty acid (FFA) release as a potential mechanism for producing stress-induced hypercholesterolemia.