Regulation of intracellular chloride activity during perfusion with hypertonic solutions in the Necturus proximal tubule.
In a previous study we presented evidence that chloride transport across the basolateral membrane in Necturus proximal tubule cells occurs predominantly via exchange for both Na+ and HCO3-. In this study the regulation of intracellular chloride was further examined in the doubly-perfused kidney preparation using conventional and chloride-sensitive microelectrodes. Application of hypertonic basolateral solutions containing 80 mM raffinose stimulated an efflux of chloride such that chloride activity remained unchanged at control levels. Membrane potential did not change in these experiments. Inhibition of Cl- exit across the basolateral cell membrane by removal of either HCO3- or Na+ from the perfusion solution resulted in a significant increase in intracellular chloride activity, aiCl, when basolateral osmolarity was raised. Hypertonic basolateral solutions also produced a significant rise in aiCl in the presence of SITS. This study provides further evidence that chloride is transported across the basolateral cell membrane in exchange for both Na+ and HCO3-. Since this exchange mechanism is activated in response to hypertonic solutions, these studies suggest a functional role for this exchanger in the regulation of aiCl in the Necturus proximal tubule cell during volume changes.
D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D001693:Biological Transport, Active / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism*; D005260:Female; D066298:In Vitro Techniques; D007424:Intracellular Fluid / Q000378:metabolism; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D008297:Male; D009337:Necturus; D010477:Perfusion; D012964:Sodium / Q000378:metabolism
D001639:Bicarbonates; D002712:Chlorides; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D012964:Sodium