the objective of this research program was to explore the effects of certain neuroendocrine mediators and macrophage function. treatment with met-enkephalin led to a flattened cell morphology with many linear and punctate microfilaments in the cytoplasm. these physical changes in cell structure were accompanied by dose-dependent increases in phagocytosis, spreading and adherence whereas cytolysis was not affected. in contrast, epinephrine treatment led to a spherical cell morphology and a dense cortical band of f-actin macrophage phagocytosis and spreading were decreased in a dose-dependent fashion whereas adherence and cytolysis were unaffected. propranolol reversed the effects of epinephrine. the effects of epinephrine were mimicked by camp analogs and forskolin combined experiments using optimal met-enkephalin doses and various doses of epinephrine gave results identical to that of epinephrine alone. these receptor signaling pathways may interact via protein kinases. protein kinase c activators and inhibitors enhance and depress macrophage spreading, respectively. cyclic amp antagonizes the action of protein kinase c activators. protein kinase systems may transduce multiple neuroendocrine signals into physiological responses via effects on granules and the cytoskeleton. keywords: stress physiology, opioid, adrenergic nerves, neurochemistry, immunology. (aw)