Recent evidence indicates that H+ extrusion in macrophages is in part accomplished by a H(+)-ATPase of vacuolar type. The presence and plasma-membrane localization of such a mechanism in adherent resident macrophages was verified by inhibition of H+ extrusion, monitored by changes in both cytosolic pH (pHi) and extracellular pH, with low concentrations of the H(+)-ATPase inhibitors N-ethylmaleimide and 7-chloro-4-nitrobenz-2-oxa-1,3-diazole. The H(+)-ATPase was operative at physiological pHi levels, thus contributing to maintenance of steady-state pHi. It was further shown to be sensitive to the plasma-membrane potential, with hyperpolarization being strongly inhibitory. In addition, H+ extrusion mediated by the H(+)-ATPase and the generation and release of lactic acid caused acidification of the pericellular space and could enable secreted lysosomal hydrolases to act extracellularly.
Research Article|January 01 1992
Cytosolic pH regulation in mouse macrophages. Proton extrusion by plasma-membrane-localized H+-ATPase
Biochem J (1992) 281 (1): 245-250.
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H Tapper, R Sundler; Cytosolic pH regulation in mouse macrophages. Proton extrusion by plasma-membrane-localized H+-ATPase. Biochem J 1 January 1992; 281 (1): 245–250. doi: https://doi.org/10.1042/bj2810245
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