The regulatory capacity of noradrenaline and its end metabolite 4-hydroxy-3-metoxyphenylglycol (HMPG) on the complete phagocytic process of macrophages were investigated. Either noradrenaline or HMPG did not modify adherence. However, 10(-12) M of noradrenaline stimulated the chemotaxis of macrophages, mainly mediated by alpha-adrenergic receptors. In contrast, 10(-12) M of HMPG induced an opposed effect on this stage of the phagocytic process. To stimulate phagocytosis, it is necessary to employ a higher concentration (10(-5) M) of noradrenaline and this effect was blocked with either 10(-6) M propranolol or 10(-6) M phentolamine, and maintained by HMPG. Noradrenaline and HMPG did not modify the microbicide capacity of macrophages (measured by O2- production after phagocytosis). In conclusion, noradrenaline modulates the phagocytic process of macrophages, and this modulation is completed by HMPG, maintaining the phagocytic functions at physiologically optimal levels. Modulation of chemotaxis is mainly mediated by alpha-receptors and phagocytosis needs both alpha- and beta-receptor-stimulation.