CHLORIDE-INDUCED INCREMENT IN SHORT-CIRCUITING CURRENT OF THE TURTLE BLADDER - EFFECTS OF INVIVO ACID-BASE STATE

Evidence for the participation of conductive and non-conductive (exchange) transmembrane anion pathways in the luminal acidification, alkalinization, and Cl-reabsorptive functions of the turtle bladder is provided from the pattern of Cl--induced changes in transepithelial electrical prameters of isolated urinary bladders from 3 groups of donor turtles: control or post-absorptive turtles (those killed 5 days after feeding); acidotic turtles (NH4Cl-loaded); and alkalotic turtles (NaHCO3-loaded). The predominance of each of the 3 aforementioned transport functions as well as the response to Cl--addition is altered by the in-vivo electrolyte balance of the turtle. In post-absorptive bladders, poised for acidification and Cl- reabsorption, the mucosal and serosal addition of Cl- to Na+-free, (HCO3- + CO2)-containing media increases the negative short-circuiting current (Isc). In aciditic bladders, poised for acidification but not Cl- reabsorption, mucosal Cl- addition has no effect on this Isc whereas serosal Cl- addition increses the negative Isc in a manner identical to that observed in the post-absorptive bladders. Alkalotic bladders do not possess an acidification function but instead are poised for Cl- reabsorption and cAMP-dependent electrogenic alkali secretion (positive Isc). In these bladders, serosal Cl- addition is without effect while mucosal Cl- addition produces transient changes in this positive Isc. These results can be replicated by a model of the turtle bladder in which transmembrane Cl- and HCO3- conductive and exchange paths mediate transepithelial acidification, alkalinization and Cl- reabsorption.