Ba2+ inhibition of electrogenic Cl- secretion in vitro frog and piglet gastric mucosa.

Gastric mucosae from frogs and newborn pigs were used for in vitro investigation of the effects of Ba2+ (10 microM to 7 mM) on transepithelial potential difference (PD), resistance and conductance (G), short-circuit current (Isc), H+ secretion, and transepithelial fluxes of 36Cl-. Ba2+ in the serosal, but not the mucosal, solution of both preparations caused PD, G, Isc, and Cl- secretion (JnetCl, Isc conditions) to decrease, while H+ secretion remained constant. Because the oxyntic cells were most likely the site of action for Ba2+, these cells must have the capacity to secrete Cl- in excess of H+ ions. The inhibitory effect of Ba2+ was not due to competition in the serosal membrane by Ba2+ for surface charges, Ca2+ sites, Na+ sites, or Cl- sites. When [K+] in both the mucosal and serosal solutions or in just the serosal solution ([K+]s) alone was increased to 10 mM, the inhibitory effects of low [Ba2+] were reduced; however, at higher [Ba2+], Isc was stimulated. At least part of the Ba2+ effect seems to be due to blockage of K+ channels in the serosal membrane of oxyntic cells. High [K+]s also caused decreased PD and Isc (but increased G) with no change in H+ secretion. It is proposed that during Isc conditions, JnetCl involves a neutral Na+-dependent accumulation of Cl- within oxyntic cells and a passive, conductive efflux fromthe cells into the mucosal solution. Ba2+ and high [K+] may alter this transport by depolarizing and, under certain conditions, hyperpolarizing intracellular voltage.