Intracellular Na+ and the control of amino acid fluxes in the integumental epithelium of a marine bivalve.

The accumulation of amino acids from sea water into the integumental epithelium of the bivalve gill can occur against chemical gradients in excess of 10(6) to 1. The energy to drive this transport has been proposed to come from the inwardly directed Na+ electrochemical gradient. The present study examined the influence of intracellular and extracellular [Na+] on influx and efflux of amino acids in gill tissue from the mussel, Mytilus californianus. Influx of alanine was inhibited by more than 90% when external [Na+] was reduced from 425 to 2 mmol l-1, and by 85% when intracellular [Na+] was increased from approximately 11 to approximately 100 mmol l-1 (by means of a 30-min exposure to the ionophore, nigericin). Efflux of taurine and alanine from gill tissue into normal-Na+ sea water was very low (less than 5% of the Jmax of the carrier-mediated influx pathways). Reducing the external Na+ from 425 to 2 mmol l-1 increased taurine efflux by only 20%. Raising cell [Na+] to approximately 100 mmol l-1 increased taurine efflux 2.7-fold; further increases in cell [Na+] increased taurine efflux another 7.5-fold. These data, in conjunction with results from earlier studies, suggest that activation of integumental amino acid transporters requires an interaction of multiple sodium ions with binding sites of low affinity for this ion. This set of characteristics results in transport systems that are well-adapted for the net accumulation of amino acids from sea water.