Conductive pathways for HCO3- in basolateral membrane of salamander intestinal cells

To understand the route of HCO3- exit across the basolateral membrane of Amphiuma small intestinal cells during active H+ secretion the influence of bath HCO3- on serosal membrane potential (Vs) was measured using conventional microelectrodes. The villus sheet preparation was used, which allowed direct access to the basal membrane for microelectrode impalement. When tissues were incubated in Cl(-)-free (SO2-4 based) medium, Vs averaged -85.8 mV. Elevation of serosal bath [HCO3-] at constant CO2 increased Vs; reduction of the [HCO3-] reduced Vs and increased the fractional resistance of the serosal membrane. When serosal bath HCO3- and CO2 were completely replaced, Vs was -44.8 mV. The serosal membrane was also depolarized on complete replacement of medium HCO3- and CO2 when bath pH was buffered with phosphate. 4,4'-Dinitro-2,2'-stilbene disulfonate (DNDS) and acetazolamide blocked the decline in Vs produced by lowering serosal medium [HCO3-]. Replacement of serosal Na+ reduced Vs 32.7 mV. DNDS blocked this response. It is concluded that a Na+-dependent, stilbene-sensitive HCO3- exit pathway resides in the basolateral membrane of the intestinal cells. Possibly there is also a parallel, conductive pathway for HCO3-.