Abstract
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).