Parallel antiport mechanisms for Na+ and Cl- transport in herbivorous teleost intestine.

Transport mechanisms for NaCl in intestinal brush border membrane vesicles (BBMV) of herbivorous, seawater-adapted tilapia, Oreochromis mossambicus, were investigated with a rapid filtration technique using 22Na+ and 36Cl- as tracers. Evidence to support the existence of cotransport mechanisms (Na+/Cl- or Na+/K+/2Cl-) in tilapia intestinal BBMV was not found. An inwardly directed Cl- gradient or KCl gradient did not stimulate the uptake of Na+ into tilapia intestinal BBMV. Furthermore, the uptake of Na+ under these conditions was not significantly affected by furosemide. Evidence was found to indicate the existence of Na+/H+ and Cl-/HCO3- antiport mechanisms for NaCl transport in tilapia intestinal BBMV. An outwardly directed proton gradient (pH 6.0 in, pH 7.5 out) stimulated the uptake of Na+ above that of the control (pH 7.5 in, pH 7.5 out). Exogenous amiloride (1 mmol l-1) significantly reduced Na+ uptake in the presence of an outwardly directed proton gradient. Apparent influxes of 1 mmol l-1 Na+ were (nmol mg protein -1 15 s-1 +/- 1 S.E.): control, 1.46 +/- 0.09; pH gradient, 3.36 +/- 0.14; pH gradient plus amiloride, 1.55 +/- 0.05. The uptake of Cl- was stimulated by outwardly directed HCO3- and Cl- gradients in comparison with an outwardly directed gluconate gradient. Apparent influxes of 10 mmol l-1 Cl- were (nmol mg protein-1 15 s-1 +/- 1 S.E.): gluconate, 12.90 +/- 0.19; HCO3-, 15.83 +/- 0.34; Cl-, 14.62 +/- 0.42. These results suggest that, in contrast to the cotransport mechanisms for NaCl that have been reported for other fish intestine, the herbivorous marine teleost, Oreochromis mossambicus, possesses dual antiport mechanisms for the transport of NaCl across its intestinal brush border membrane.