INABILITY OF CA2- STUDIES WITH FURA-2 AND SBFI MICROFLUOROMETRY( INFLUX THROUGH NICOTINIC ACH RECEPTOR CHANNELS TO STIMULATE CATECHOLAMINE SECRETION IN BOVINE ADRENAL CHROMAFFIN CELLS )

The concentration of cytosolic Ca2+ ([Ca](in)) and catecholamine (CA) secretion were examined in bovine adrenal chromaffin cells to determin e whether Ca2+ influx through nicotinic ACh receptor (nAChR) channels contributes to CA secretion induced by nAChR stimulation. Nicotine add ed under Na+-free conditions caused a marked increase in [Ca](in) and quenching of fura-2 fluorescence in the presence of Mn2+ suggesting th e stimulated entry of divalent cations through nAChR channels. However , nicotine-induced increase in CA secretion occurred only at a non-phy siologically high external Ca2+ concentration under Naf-free condition s. Both the nicotine-induced increase in [Ca](in) and CA secretion und er Na+-free conditions were reduced in the presence of hexamethonium, methoxyverapamil (D600), nifedipine, Bay-K-8644, clonidine, and guanet hidine. All of these agents inhibited the nicotine-induced increase in cytosolic Na+ concentration in a dose-dependent manner, as measured b y SBFI microfluorometry. The present results suggest that Ca2+ influx through nAChR channels under physiological conditions may not contribu te to CA secretion.