Abstract
Adrenergic responses during normoxia and chemical anoxia were investigated in anoxia‐tolerant hepatocytes from the goldfish, Carassius auratus. Epinephrine‐stimulated glucose release was unaltered after 1 hr of chemical anoxia, the concentration of epinephrine required for half maximal stimulation of glucose release (K) ranging from 0.62 × 10^–8^ to 2.05 × 10^–8^ M. Similarly, the maximum rate of glucose release caused by hormonal stimulation was not affected by chemical anoxia. In anoxic goldfish hepatocytes [Ca^2+^]~i~ remained constant in nonstimulated cells but could be elevated by addition of epinephrine. The magnitude of this [Ca^2+^]~i~‐increase was dependent on the concentration of the catecholamine and this dependency was similar under normoxia (K = 1.17 × 10^–8^ M) and chemical anoxia (K = 1.15 × 10^–8^ M), as was the percentage of cells responding (77%) and displaying oscillatory [Ca^2+^]~i~ response patterns (60%) after epinephrine addition, although the frequency of [Ca^2+^]~i~ oscillations was significantly lower in anoxic cells. To analyze a possible shift in the importance of α‐ and β‐adrenoceptors during chemical anoxia, the effect of phentolamine and propranolol, α‐ and β‐adrenergic antagonists respectively, on epinephrine‐stimulated glucose release was studied. Application of the α‐antagonist caused a dose‐dependent reduction of glucose‐release which was similar under both conditions, whereas the sensitivity to the β‐antagonist was lowered after chemical anoxia. Taken together these results provide evidence that during chemical anoxia goldfish hepatocytes remain responsive to adrenergic stimulation and that there is a partial shift regarding the contribution of α‐ and β‐adrenergic pathways to the induction of cellular glucose release stimulated by epinephrine. J. Exp. Zool. 292:468–476, 2002. © 2002 Wiley‐Liss, Inc.