Abstract

Fluid transport and net fluxes of Na, K, Cl and HCO3 by guinea pig gallbladder were investigated in vitro. A perfused gallbladder preparation was devised to simultaneously study unidirectional fluxes of 22Na and 36Cl. The net Cl flux exceeded the net Na flux during fluid absorption in the presence of HCO3. This Cl excess was counterbalanced by a net HCO3 secretion: a HCO3-Cl exchange. PGE1 reversed the direction of fluid transport and abolished the net Cl flux. The magnitude of the HCO3 secretion remained unchanged, but shifted from a HCO3-Cl exchange to a net secretion of NaHCO3 and KHCO3. Furosemide inhibited both the HCO3-Cl exchange and HCO3 secretion after PGE1 without influencing fluid absorption. Ouabain inhibited the HCO3-Cl exchange as well as fluid absorption; only the effect on the HCO3 secretion was entirely reversible. Secreted HCO3 appeared not to be derived from metabolic sources since HCO3 secretion was abolished in a HCO3-free bathing medium. HCO3 secretion was also dependent on the Na concentration of the bathing fluid. Three lines of evidence are presented in favor of an active HCO3 secretion in guinea pig gallbladder. HCO3 is secreted against: (i) a chemical gradient, (ii) an electrical gradient and (iii) the direction of fluid movement under control conditions.

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