SUMMARY1. The addition of isoprenaline to an isotonic suspension of red blood cells of rainbow trout induces an amiloride-sensitive Na+ transport which is independent of Cl-and insensitive to 4,4'-diisothiocyano-2,2'-stilbene disulphonic acid (DIDS) and furosemide.2. Na+ uptake is accompanied by amiloride-sensitive H+ release. The H+ efflux is dependent upon the external Na+ concentration, the Ko.5 value for Na+ being 16 mm.3. In the presence of DIDS, when the coupled NaCl entry (NaCl co-transport) induced by catecholamine is blocked, the results provide evidence for a linked movement of Na+ and H+, with a stoicheiometry of 1 :1.4. Exchange of H+ for Na+ induces osmotic swelling of the cells which is due to the replacement of a bound proton by an osmotically active Na+ cation.5. In the absence of DIDS when the bulk of the Na+ uptake is the result of a coupled entry of Na+ and Cl-, H+ extrusion still occurs and the magnitude of acid excretion is identical to that found in DIDS-treated cells. This suggests that Na+-H+ exchange remains active.6. Addition of isoprenaline first stimulates the Na+-H+ exchange but only transiently. This is followed by a more permanent stimulation ofthe NaCl co-transport.

On the addition of isoprenaline to an isotonic suspension of red blood cells of rainbow trout (Salmo gairdneri), the cell volume increases. This increase in volume is the result of net uptake of Na+ and osmotically obligated water. Two different pathways are involved in the salt uptake. The minor component of Na+ entry (about 20%) corresponds to a Na+ uptake independent of Cl‐ and is inhibited by amiloride, yet is insensitive to DIDS, furosemide and niflumic acid. It could result from Na+/H+ countertransport. The major component of salt uptake is due to Na+ entry which requires Cl‐ as anion, and is electroneutral, independent of extracellular K+, sensitive to amiloride, DIDS, niflumic acid and furosemide, but insensitive to other loop diuretics such as piretanide or bumetanide. These characteristics, as well as the response of valinomycin‐treated cells to isoprenaline and some other properties (ionic selectivity, drug sensitivity) of the anion exchange system of volume‐static trout red cells, permit the definition of the nature of this Cl‐‐dependent pathway. The findings are inconsistent with the electrically silent double antiporter model (proposed in amphibian red cells by Cala, 1980) and with the co‐migration of Cl‐ with Na+ through parallel conductive pathways, but strongly suggest a symport mechanism. Striking differences, mainly pharmacological, exist between this NaCl co‐transport and the duck red blood cell Na+/K+/2Cl‐ co‐transport (Kregenow, 1977, 1978; McManus & Schmidt, 1978).