Black bullhead catfish (Ameiurus melas) were exposed to air for 1 h to examine the effect of an acute stress on the distribution and function of the hepatic beta-adrenoceptors (beta-ARs). Air exposure significantly reduced both adrenaline (ADR)- and noradrenaline (NADR)-stimulated glucose production in isolated hepatocytes with no effect on either receptor affinity (K(d)) or number of binding sites (B(max)). A 24 h exposure of isolated hepatocytes to the beta-agonist isoproterenol also had no significant impact on either binding parameter. Competition studies using selective agonists and antagonists suggest that the hepatic beta-AR in this species is pharmacologically beta(2)-like. However in addition to the beta(2)-AR, molecular evidence provides support for the existence of hepatic beta-ARs that phylogenetically group with the beta(3)-ARs and the beta(1)-ARs. Despite the presence of several potential phosphorylation sites in the third intracellular loop and cytoplasmic tail of the bullhead beta(2)-AR, no significant changes were observed in the binding parameters. While physiological data supports the presence of only a single subtype, molecular data supports the existence of multiple beta-AR subtypes in this species. The mechanisms thought to regulate mammalian beta-ARs exist in the bullhead ARs reported here but these mechanisms are not as effective in this fish system as in mammals.