Isoprenaline, histamine and PGE1 inhibit N-formylmethionyl-leucyl-phenylalanine evoked lysosomal enzyme release from human neutrophils. Their effects are dose-dependent and potentiated by 3-isobutyl-1-methylxanthine pretreatment of the cells. The order of activity is PGE1 greater than isoprenaline greater than histamine. The maximum of inhibition afforded by each agonist depends on the amount of the secretory stimulus, since it is higher at lower concentrations of the secretagogue. Isoprenaline effects are competitively antagonized by propranolol and are mimicked by fenoterol and salbutamol. These results suggest that human neutrophil functions are modulated by endogenous control mechanisms, that can also be activated by drugs acting on the same receptors as the endogenous mediators.