Adult catfish, Ictalurus melas, hepatocytes respond to alpha-agonists by increasing intracellular free calcium concentrations ([Ca2+]i) in a dose-dependent manner. Basal [Ca2+]i were approximately 78 nM in catfish hepatocytes; this value was increased by 213, 243, 131, and 238 nM in the presence of epinephrine (Epi; 10(-6) M), norepinephrine (NE; 10(-5) M), phenylephrine (PE; 10(-4) M), and isoproterenol (Iso; 10(-4) M), respectively. The binding constants were 3.4 x 10(-8), 2.6 x 10(-7), 9.8 x 10(-7), and 6.1 x 10(-5) M for Epi, NE, PE, and Iso, respectively, which is the same order of potency for these agonists reported for the alpha 1-adrenoceptor system of mammalian hepatocytes. The Epi-induced changes in [Ca2+]i were antagonized equally by phentolamine (PH; 10(-8) M) and yohimbine (10(-8) M) but poorly by propranolol (Prop; 10(-6) M), as indicated by their respective inhibitory constants. Epi (10(-7) M) induced a time-dependent increase in hepatocyte adenosine 3',5'-cyclic monophosphate concentration that was antagonized by Prop but not PH. There were, however, no clear agonist-induced changes in the activities of glycogen phosphorylase (total, a, or %a) under these conditions. These studies provide evidence that Epi and other adrenergic agonists increase [Ca2+]i by an alpha- or alpha 1-like adrenoceptor pathway in catfish hepatocytes, but the biochemical effector system responding to changes in [Ca2+]i has yet to be elucidated.