Abstract
The normal internal pH (pH i) of the amphibian lens, measured using ion-sensitive microelectrodes, is 7·1 (pH o = 7·4) and the membranes appear to be relatively impermeable to hydrogen ions. Perifusing the lens with 100% CO 2 appeared to be the most efficient way of decreasing pH i, which fell to 6·3 after an exposure lasting 30 min. Accompanying this acidification, there was a rapid depolarization of membrane potential ( E m), a decrease in membrane resistance ( R m) and increase in internal or bulk resistance ( R i). These changes did not occur if the external pH alone was decreased. All changes were reversible, although the time course of R i recovery was faster than the others. The decrease in membrane resistance could be prevented if the chloride concentration in the external solution was reduced, suggesting that internal acidification opens chloride channels in the amphibian lens. Since chloride ions are normally close to equilibrium across amphibian lens membranes, it is suggested that the pH-induced depolarization is due to a decrease in potassium conductance. The increase in internal resistance on perifusing with CO 2 is most likely due to a closing of gap junctions between the fibre cells. The relationship between internal conductance and pH i was very similar to that obtained in other tissues and could be fitted by the Hill equation with n = 6 and pK = 6·9. Fibre junctional conductance seems sensitive to small changes in hydrogen ion concentration around the resting pH. Two agents, aspirin and cyanate, that are believed to influence cataract development, slowed the recovery of E m, R m and R i during recovery from an acid load. Neither of these agents influenced R i when applied in control solution, although aspirin hyperpolarized the membrane potential and cyanate depolarized the potential.
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