Stimulation by HCO3- of Na+ transport in rabbit gallbladder.
Bicarbonate presence in the bathing media doubles Na+ and fluid transepithelial transport and in parallel significantly increases Na+ and Cl- intracellular concentrations and contents, decreases K+ cell concentration without changing its amount, and causes a large cell swelling. Na+ and Cl- lumen-to-cell influxes are significantly enhanced, Na+ more so than Cl-. The stimulation does not raise any immediate change in luminal membrane potential and cannot be due to a HCO3(-)-ATPase in the brush border. The stimulation goes together with a large increase in a Na+-dependent H+ secretion into the lumen. All of these data suggests that HCO3- both activates Na+--Cl- cotransport and H+--Na+ countertransport at the luminal barrier. Thiocyanate inhibits Na+ and fluid transepithelial transport without affecting H+ secretion and HCO3(-)-dependent Na+ influx. It reduces Na+ and Cl- conentrations and contents, increases the same parameters for K+, causes a cell shrinking, and abolishes the lumen-to-cell Cl- influx. It enters the cell and is accumulated in the cytoplasm with a process which is Na+-dependent and HCO3(-)-activated. Thus SCN- is likely to compete for the Cl- site on the cotransport carrier and to be slowly transferred by the cotransport system itself.
D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology*; D001693:Biological Transport, Active / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D004848:Epithelium / Q000378:metabolism; D005704:Gallbladder / Q000378:metabolism*; D006859:Hydrogen / Q000378:metabolism; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D012964:Sodium / Q000378:metabolism*; D013861:Thiocyanates / Q000494:pharmacology; D014867:Water / Q000378:metabolism
D001639:Bicarbonates; D002712:Chlorides; D013861:Thiocyanates; D014867:Water; D006859:Hydrogen; D012964:Sodium; D011188:Potassium