Abstract
The contribution of chloride ion movement and sodium and bicarbonate concentrations to the net current across the isolated choroid-retinal pigment epithelium (RPE) of the bullfrog were studied. The presence of a ouabain-sensitive Na + K + -pump on the retinal side was confirmed and complete inhibition of this pump with Na + removal and ouabain treatment abolished nearly all the RPE transepithelial transport and SCC suggesting that all ionic transport was dependent on sodium. It was found that apical to basal (AB) chloride flux accounted for 26±2% (mean± s.e.m.) of the short circuit (SCC). Results suggest that AB bicarbonate and/or basal apical (BA) hydrogen ion net transport accounts for 38±2% of the SCC while BA sodium is presumably responsible for the remaining 34% of the SCC. Transport was inhibited by apical administration of known chloride inhibitors. Trans-RPE 36Cl flux measurements indicate that furosemide (10 −4 m), bumetanide (10 −4 m) and SITS (10 −3) decrease the retinal-choroid flux. Results suggest that net transport of chloride and bicarbonate are independent of each other and additive. It was found that a bicarbonate-free preparation was relatively unaffected by changes in pH (5·5–8·5) indicating that pH has little, if any, effect on sodium or chloride current in this range. A model is presented which is compatible with the various data. It is suggested that along with the apical Na + K + -ATPase pump, there exists an apical Na + Cl − -co-transport system which is driven by the established sodium gradient. Moreover, this pump established sodium gradient is postulated to drive a Na + HCO 3 − -co-transport system tentatively placed on the retinal side of the RPE.
Published Version
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