To examine the modulatory effects of catecholamines on the respiratory burst in polymorphonuclear leukocytes (PMNs), dopamine was tested for its capacity to modify the superoxide anion (O2-) production by PMNs under their stimulation with several stimuli. Dopamine inhibited the O2- production by PMNs when PMNs were stimulated with N-formylated chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP), phorbol myristate acetate, or opsonized zymosan, whereas dopamine did not alter the PMN mobility. The values of percentage inhibition of the O2- production by FMLP-stimulated PMNs were 57% under treatment with 10(-5) mol/L and 83% with 10(-4) mol/L of dopamine. Isoproterenol also inhibited PMN O2- production in response to FMLP. Although a beta-adrenergic blockade, propranolol, diminished the isoproterenol-induced inhibition of the O2- production, it did not affect the inhibitory effect of dopamine. The increase in intracellular cyclic AMP levels in dopamine-treated PMNs was much smaller than the increase in isoproterenol-treated cells. Furthermore, dopamine inhibited the reduced nicotinamide-adenine dinucleotide phosphate-dependent O2- production by subcellular particles. These results indicate that dopamine inhibits PMN O2- production through its effect on PMN reduced nicotinamide-adenine dinucleotide phosphate-oxidase system rather than through its beta-adrenergic action.