Active chloride transport powered by Na-K-ATPase in shark rectal gland.

Abstract

The isolated rectal gland of the spiny dogfish is a unique model for the study of active chloride transport. The gland is stimulated to secrete chloride agains an electrical and a chemical gradient when perfused in vitro by theophylline and/or dibutyryl cyclic AMP. Chloride secretion is depressed by ouabain which inhibits Na-K-ATPase. Thiocyanate and furosemide also inhibit chloride secretion but ethoxolamide, a carbonic anhydrase inhibitor, does not. Chloride transport is highly dependent on sodium concentration in the perfusate. The intracellular concentration of chloride in intact glands exceeds the level expected at electrochemical equilibrium, suggesting active transport of chloride into the cell. These features suggest a general hypothesis for chloride secretion in which the uphill transport of chloride into the cytoplasm is coupled through a membrane carrier to the downhill movement of sodium along its electrochemical gradient. The latter is maintained by the Na-K-ATPase pump while chloride is extruded into the duct by electrical forces.