Russell J M, Boron W F, Brodwick M S
J Gen Physiol. 1983 Jul;82(1):47-78. doi: 10.1085/jgp.82.1.47.
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 mechanism that exchanges external Na+ and HCO-3 for internal Cl- and possibly H+. However, we found that net transport can be reversed either by lowering [HCO-3]o and pHo or by reducing [Na+]o. This reversal (acid uptake) required external Cl-, was stimulated by raising [Na+]i, and was blocked by SITS. When the transporter was operating in the net forward direction (acid extrusion), we found a unidirectional Na+ influx of approximately 60 pmol . cm-2 . s-1, which required external HCO-3 and internal Cl- and was stimulated by cyclic AMP and blocked by SITS or DIDS. These properties of the Na+ influx are all shared with the net acid extrusion process. We also found that 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 in the net forward direction, mediates a small amount of reversed transport. We also found that the ouabain-sensitive Na+ efflux was sharply inhibited by acidic pHi, being totally absent at pHi values below approximately 6.8.
通过测量内部透析纤维中的细胞内pH值（pHi）和单向Na⁺通量，研究了调节巨型藤壶肌纤维细胞内pH值（pHi）的离子转运机制。通常情况下，整个过程会导致细胞净排出酸，推测是通过一种膜转运机制，该机制将外部Na⁺和HCO₃⁻与内部Cl⁻以及可能的H⁺进行交换。然而，我们发现通过降低[HCO₃]ₒ和pHₒ或降低[Na⁺]ₒ，净转运可以逆转。这种逆转（酸摄取）需要外部Cl⁻，通过提高[Na⁺]ᵢ来刺激，并被SITS阻断。当转运体正向净运转（酸排出）时，我们发现单向Na⁺内流约为60 pmol·cm⁻²·s⁻¹，这需要外部HCO₃⁻和内部Cl⁻，并受到环磷酸腺苷的刺激，被SITS或DIDS阻断。Na⁺内流的这些特性与净酸排出过程相同。我们还发现，在正向净转运条件下，pHi调节系统介导了单向Na⁺外流，其明显小于同时发生的Na⁺内流。这些数据与一种可逆转运机制一致，即使在正向净运转时，该机制也介导少量的逆向转运。我们还发现，哇巴因敏感的Na⁺外流受到酸性pHi的强烈抑制，在pHi值低于约6.8时完全不存在。
