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AJP - Cell Physiology, Vol 254, Issue 3 C391-C396, Copyright © 1988 by American Physiological Society
ARTICLES |
R. J. Turner and J. N. George
Clinical Investigations and Patient Care Branch, National Institute of Dental Research, Bethesda, Maryland 20892.
The presence of a sodium-independent electroneutral Cl(-)-anion exchanger in a basolateral membrane vesicle preparation from the rabbit parotid is demonstrated. This exchanger is shared by HCO3-, NO3-, Br-, F-, and formate, but not by thiocyanate, acetate, methylsulfate, gluconate, or hydroxyl ions. In order of relative potency, the exchanger is inhibited by SITS greater than or equal to phloretin greater than furosemide greater than bumetanide greater than or equal to phlorizin. A Na+-K+-dependent component of chloride flux, presumably due to the Na+-K+-Cl- cotransporter already characterized in this preparation, was also observed. 36Cl uptake into vesicles loaded with KCl exhibited an "overshoot" of intravesicular [36Cl] due to 36Cl-Cl exchange. However, when vesicles were loaded with both KCl and NaCl the height of the overshoot was considerably decreased indicating a Na+-K+-dependent dissipation of the intravesicular to extravesicular chloride gradient. This experiment provides strong evidence that the Na+-K+-Cl- cotransporter and the Cl(-)-HCO3- exchanger are present in the same membrane vesicles. These results indicate that Cl(-)-HCO3- exchange is present in the basolateral membrane of parotid acinar cells and thus that this transporter may play a significant role in salivary secretion.
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