ACETAZOLAMIDE-SENSITIVE SHORT-CIRCUITING CURRENT VERSUS MUCOSAL HCO3- CONCENTRATION IN TURTLE BLADDERS

Isolated bladders of Pseudemys turtles, interposed between choline sulfate Ringer solution on the mucosa and choline sulfate Ringer solution with HCO3- (20 mM) on the serosa were short-circulated in a chamber. Mucosal concentration of HCO3- was varied from 0.2 to 20 mM in the presence and in the absence of acetazolamide. Both in the presence and in the absence of acetazolamide, spontaneous trans-bladder potential and short-circuiting current (Isc) increased with increasing mucosal HCO3- concentration. When Isc was plotted as a function of mucosal HCO3- concentration, it exhibited Michaelis-Menten-like characteristics. In the absence of acetazolamide, the saturation current and half maximal concentration of mucosal HCO3- were 1.98 mA/g dry tissue and 2.4 mM HCO3-, respectively. In the presence of 0.1 mM acetazolamide, they were 0.37 mA/g dry tissue and 3.15 mM HCO3-, and in the presence of 0.2 mM acetazolamide they were 0.24 mA/g dry tissue and 3.89 mM HCO3-. The changes in the half maximal concentration of mucosal HCO3- were not significant. Hence, acetazolamide appears to inhibit HCO3- transport in a manner analogous to noncompetitive inhibition. Data further indicate that the inhibition of HCO3- transport by acetazolamide is reversible. Analysis of data from experiments carried out in the absence of acetazolamide suggest the existence of a second HCO3- transport process having a saturation current of 1.13 mA/g dry tissue and a half maximal concentration of 0.17 mM HCO3- in the mucosal fluid. © 1969.