By microdialysis in the unilateral caudal ventrolateral medulla (CVLM) of anesthetized rats, the spontaneous l-3,4-dihydroxyphenylalanine ( l-DOPA) release was in part tetrodotoxin-sensitive or Ca 2+-dependent and was abolished by i.p. α-methyl- p-tyrosine (α-MPT), a tyrosine hydroxylase inhibitor. High K + (50 mM) Ca 2+-dependently evoked l-DOPA. By unilateral microinjections into the CVLM, l-DOPA (10–100 ng) produced dose-dependent, marked hypotension and bradycardia similarly in rats untreated, treated with i.p. 3-hydroxybenzylhydrazine, a central DOPA decarboxylase inhibitor, or with i.v.t. 6-hydroxydopamine. These responses were antagonized by l-DOPA methyl ester, a competitive l-DOPA antagonist. A depressor response to dopamine or noradrenaline (100 ng) was far smaller and slower in onset than that to l-DOPA (30 ng). d-DOPA (100 ng) produced no effect. Furthermore, l-DOPA methyl ester microinjected into bilateral CVLM produced some hypertension and tachycardia, which were markedly reduced by α-MPT. Transmitter-like l-DOPA tonically functions to mediate vasodepressor control in CVLM of rats.