Small doses of epinephrine (0.008, 0.05, and 0.1 pmol, i.e., 20-nl volumes of 0.40, 2.5, and 5 microM solutions) produced a dose-dependent increase in heart rate when micro-injected into the right intermediolateral column (IML) at T2 spinal level. These effects were mediated via alpha 1-adrenergic receptors because prazosin blocked them. The presence of alpha 1-adrenergic receptors at this site was confirmed by microinjections of phenylephrine (a specific agonist for these receptors); phenylephrine elicited tachycardia. Larger doses of epinephrine (320, 2,000, and 3,200 pmol, i.e., 20-nl volumes of 16, 100, and 160 mM solutions) caused bradycardia when microinjected into the IML. These effects were mediated via alpha 2-adrenergic receptors because idazoxan blocked them. The presence of alpha 2-adrenergic receptors at this site was confirmed by microinjections of clonidine (a specific agonist for these receptors); clonidine elicited bradycardia. Injections of the vehicle (20 nl of normal saline containing 0.3% ascorbic acid, pH 7.4) did not evoke a response. Epinephrine, prazosin, or idazoxan did not alter the responses to L-glutamate. None of the doses of epinephrine elicited any response when injected intravenously. The aforementioned results provide pharmacological evidence for the presence of alpha 1- and alpha 2-adrenergic receptors in the IML at T2. Thus a basis is provided for investigating the role, if any, of alpha-adrenergic receptors in the IML in mediating cardiovascular responses elicited by the stimulation of different brain stem areas.