The mechanisms of inhibition of branchial ion transport by epinephrine and somatostatin were investigated in the isolated perfused gill preparation of seawater-adapted flounder Platichthys flesus. The electrogenic transepithelial potential recorded in gills perfused and bathed with identical salines was stimulated by glucagon, forskolin, or a cyclic adenosine 5' monophosphate (AMP) derivative, each administered at a concentration identified in preliminary experiments as being submaximally effective. The subsequent abilities of epinephrine and somatostatin to inhibit the stimulated potential were found to be dependent on the site of action of the stimulatory agent with respect to the formation of cyclic AMP. Thus the maximal adrenergic or peptidergic inhibition of the potential stimulated by exogenous cyclic AMP was significantly reduced compared with the maximal inhibition of the potential stimulated by either forskolin or glucagon. The data indicate dual modes of action by which epinephrine and somatostatin achieve maximal inhibition of branchial ion transport; a cyclic AMP-independent mechanism that is effective in the presence of cyclic AMP and an additional mechanism to inhibit cyclic AMP synthesis.
Animals Biological Transport