Mechanisms of chloride transport in thymic lymphocytes

Abstract

This study examined mechanisms of Cl- transport in rat lymphocytes under a variety of conditions. Basal intracellular Cl- concentration ([Cl-]i) was not different between cells assayed in the presence of HCO3- or its absence (HEPES). Removal of external Cl- resulted in a fall in [Cl-]i and a rapid rise in intracellular pH (pH(i)). Both Cl- efflux and the rise in pH(i) were blocked by DIDS or removal of external Na+ but were unaffected by furosemide. The mechanisms governing Cl- influx were assessed in cells that had been Cl- depleted for 1 h. Reexposure to Cl- resulted in a rapid rise in [Cl-]i that was partially inhibited by pretreatment with DIDS (57%) and partially inhibited by pretreatment with furosemide (45%). Pretreatment with both compounds together completely blocked Cl- influx. Cl- depletion caused a marked increase in pH(i) that rapidly declined toward normal when the cells were reexposed to Cl-. Preincubation with DIDS completely blocked this decrease in pH(i). In contrast, neither removal of Na+ nor preincubation with furosemide affected the decline in pH(i) when the cells were reexposed to Cl-. We conclude that, in thymic lymphocytes, Cl-/HCO3- (or Cl-/base exchange) regulates both Cl- influx and efflux. Cl- efflux is totally inhibited by DIDS and is mediated by a Na+-dependent Cl-/HCO3- exchanger. Cl- influx is partially DIDS sensitive and partially furosemide sensitive and is mediated by both a Na+-independent Cl-/HCO3- exchanger and by a Na+-K+-2Cl- cotransporter.

The Divergence, Actions, Roles, and Relatives of Sodium-Coupled Bicarbonate Transporters

“…Stakisaitis et al (903) report that Na ϩ -dependent Cl-HCO 3 exchange is responsible for the net Cl Ϫ efflux, measured as a fall in [Cl Ϫ ] i , observed when cells are bathed in a solution lacking Cl Ϫ (903). However, this result is not consistent with the phenotype of human NDCBE heterologously expressed in Xenopus oocytes: human NDCBE mediates a 36 Cl efflux only in the presence of extracellular Cl Ϫ (719).…”

Effects of furosemide on allergic asthmatic responses in mice

“…Indeed, the Ca 21 -activated Cl À channel (CaCC) and Atype g-aminobutyric acid receptor (GABA A R) are also expressed in AECs [10,11] and ASM [12,13]. Moreover, NKCC1 has been identified on the T lymphocyte [14], a key player in the pathogenesis of allergic diseases. These findings suggest that increased sensitivity of ASM and/or phenotypic transformation of AEC as potential effects of NKCC activation in the pathogenesis of asthma [15].…”

Sodium valproate stimulates potassium and chloride urinary excretion in rats: gender differences

“…Intracellular Cl - level and Cl - transport differences could be important in the regulation of cellular processes and could help to explain certain functional differences of cells [9,10]. Cl - is an important factor of intracellular pH [11], which is involved in the complex of cell function regulation.…”