A pharmacological analysis of chloride transport across the amphibian cornea.

1. Active Cl, but not Na, transport across the toad cornea was inhibited by mepacrine, which is a phospholipase A2 inhibitor; trifluoperazine, which blocks the action of calmodulin; and meclofenamic acid, which inhibits synthesis of prostaglandins. Bumetanide and DIDS (4,4'-diisothiocyano-2,2'-stilbene disulphonic acid) have previously been shown to inhibit this Cl transport. The interactions of these antagonists with several agonists that increase Cl transport were studied. 2. The effects of adrenaline, prostaglandin E2, dibutyryl cyclic AMP (DBcAMP) and the Ca ionophore A23187 were inhibited by mepacrine, trifluoperazine and bumetanide. 3. The inhibitory effects of high concentrations of DIDS, however, could be overcome by all of the agonists except DBcAMP. 4. Meclofenamic acid only blocked the effects of A23187. 5. A model is proposed to account for the observed actions and interactions of the various antagonists and agonists on Cl transport. This involves possible roles for Ca, calmodulin and phospholipase A2.