Abstract
The mechanism of Cl - secretion in the isolated, resting (i.e. cimetidine-treated) gastric mucosa of Necturus has been investigated with radioisotopic and electrophysiological techniques. Measurement of transepithelial 36 C1 - fluxes (mucosal to serosal (M→S), J Cl - ms ; S→M, J Cl - sm ) during control conditions show that at open circuit, when the transepithelial potential difference Ψ ms = 20 mV (S ground), J Cl - ms = J Cl - sm , i.e. J Cl - net = 0, but during short-circuit current conditions J Cl - net = I sc = 2 μ equiv cm -2 h. Experiments with low [Cl - ] solutions indicate that Cl - exchange diffusion does not contribute significantly to either J Cl - ms or J Cl - sm . Double-barrelled, Cl - -selective microelectrodes showed that in open circuit, the cellular (C) chemical potential for Cl - , Ψ Cl - e = 31 mV (apparent [Cl - ] = 29 mM), the electrical potential across the M membrane, Ψ m = — 34 mV (mucosa ground) while that across the S membrane, Ψ s = — 52 mV (serosa ground). During short-circuit current conditions, Ψ m = Ψ s = —49 mV and [Cl - ] e = 30 mM. The permeability of the M membrane to Cl - ( Ρ Cl - m ) was calculated both from the tracer experiments and the electrode measurements by using the constant-field equation. Short-term (45 s) uptake of 36 Cl - at [Cl - ] m = 96 mM during short circuit conditions gave Ρ Cl - m = 2.6 x 10 -5 cm s -1 . Measurement of [Cl - ] c by means of the electrodes when [Cl - ] m was changed from 96 to 2 mM or from 2 to 96 mM gave Ρ Cl - m = 2.9- 5.7 x 10 -5 cm s -1 . Our results indicate that during open circuit conditions Cl - is accumulated across the S membrane into gastric cells in an energy-requiring step, but since J Cl - net = 0, Cl - must leak back into the S solution at a rate equal to the entry rate. When the tissue is short-circuited, Cl - secretion occurs ( J Cl - net = I sc ) owing to the same energy-requiring accumulation of Cl - by the cells and a passive (apparently electrodiffusive) movement across the mucosal membrane.