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Towards an estimate of chloride permeability in the smooth muscle of guinea‐pig vas deferens.

Cl movements across the cell membranes of smooth muscle from the guinea‐pig vas deferens were measured using Cl‐sensitive micro‐electrodes and 36Cl fluxes. The rate constants for the loss of Cl ions measured by both methods under a variety of conditions were used to calculate the apparent Cl permeability (PCl). If it is assumed that the initial rate of decline of the intracellular Cl activity (aiCl) on removal of extracellular Cl (Clo) represents net transmembrane Cl movement, the apparent PCl was 3‐6 X 10(‐8) cm s‐1. This value is in good agreement with those calculated from the rate constant of 36Cl efflux into both normal Krebs solution (steady‐state) and Cl‐free solution. Such a value for PCl predicts a large depolarization on removal of Clo, but only a minimal change was recorded. It also predicts that changes in membrane potential (Em) would affect aiCl; furthermore that removal of Clo would increase membrane resistance and thus the hyperpolarization observed on reactivation of the electrogenic Na pump. Neither of these was observed. The PCl/PK ratio obtained from changes in Em on rapid changes in Clo and Ko gives a value for PCl which is an order of magnitude lower: 4 X 10(‐9) cm s‐1, using Casteels' (1969 b) value for PK. These observations can be reconciled by a substantial proportion of the measured Cl movements being carrier‐mediated. The presence of the stilbene derivative DIDS greatly slowed both the steady‐state efflux and uptake of 36Cl, as has previously been shown for the loss and reaccumulation of Cl ions on removal and replacement of Clo. PCl calculated in the presence of DIDS was about 5 X 10(‐9) cm s‐1. The nominal absence of CO2 and HCO3, which slows the reaccumulation and loss of Cl, had no effect on the steady‐state fluxes. This indicates that the carrier operates in the self‐exchange mode in the steady state.