Intracellular pH and Na fluxes in barnacle muscle with evidence for reversal of the ionic mechanism of intracellular pH regulation.

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Abstract
The ion transport mechanism that regulates intracellular pH (pHi) in giant barnacle muscle fibers was studied by measuring pHi and unidirectional Na+ fluxes in internally dialyzed fibers. The overall process normally results in a net acid extrusion from the cell, presumably by a membrane transport mechnaism that exchanges external Na+ and HCO3- for internal Cl- and possibly H+. Net transport can be reversed either by lowering [HCO3-]0 and pH0 or by reducing [Na+]0. This reversal (acid uptake) required external Cl-, was stimulated by raising [Na+]i, and was blocked by SITS [4-acetoamidoisothiocyanatostilbene-2,2''-disulfonic acid]. When the transporter was operating in the net forward direction (acid extrusion). A unidirectional Na+ influx of .apprx. 60 pmol .cntdot. cm-2 .cntdot. s-1 was found which required external HCO3- and internal Cl- and was stimulated by cAMP and blocked by SITS or DIDS [4,4''-diisothiocyano-2,2''stilbenedisulfonic acid]. These properties of the Na+ influx are all shared with the net acid extrusion process. Under conditions of net forward transport, the pHi-regulating system mediated a unidirectional Na+ efflux, which was significantly smaller than the simultaneous Na+ influx. These data are consistent with a reversible transport mechanism which, even when operating the net forward direction, mediates a small amount of reversed transport. The ouabain-sensitive Na+ efflux was sharply inhibited by acidic pHi, being totally absent at pHi values below .apprx. 6.8.