Chloride and taurine effluxes occur by different pathways in skate erythrocytes. Davis-Amaral, Erin M., Mark W. Musch, and Leon Goldstein. Department of Physiology, Brown University, Providence, RI 02912, Department of Medicine, Inflammatory Bowel Disease Research Center, University of Chicago, Chicago, IL 60637, Mount Desert Island Biological Laboratory, Salsbury Cove, Maine 04672
APStracts 3:0249R, 1996.
The aim of this study was to determine whether volume-activated taurine and chloride effluxes occurred via the same system in skate (Raja erinacea) red blood cells (RBC). The effluxes were measured in isotonic and hypotonic elasmobranch Ringer solutions in which NaCl was replaced by mannitol and the remaining exchangeable anions with gluconate. 0.1mM methazolamide was added to minimize HCO3- formation. RBC Cl- content fell about 50%/h in both isotonic and hypotonic media, with no detectable K+ loss in either media. The observed Cl- loss was accompanied by an increase in pH. Both the Cl- loss and pH rise were inhibited by DIDS (0.1mM), suggesting that Cl- efflux was due to H+/Cl- cotransport. 36Cl- effluxes in isotonic and hypotonic media were (mean +/- S.E., n=11) 2.8 +/- 0.6 [mu]mol/g x DW RBC x min and 3.5 +/- 0.9, respectively while 3H-taurine effluxes in the same media were 0.045 +/- 0.02 [mu]mol/g x DW RBC x min (n=6) and 2.1 +/- 0.05. These results indicate that taurine and Cl- effluxes occur via different pathways in skate RBC. In addition, the swelling-activated chloride channel reported in epithelial cells does not appear to be present in skate RBC. This conclusion was confirmed by Western blots with an antibody to swelling-activated chloride channels. Taurine and Cl- fluxes are apparently under different pathway influences in these RBC: taurine diffuses via a channel while Cl- is transported by cotransporters. 

Received 25 January 1996; accepted in final form 15 May 1996.
APS Manuscript Number R44-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96