Cell membrane potential: a signal to control intracellular pH and transepithelial hydrogen ion secretion in frog kidney

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Abstract
The dependence of intracellular pH (pHi) and transepithelial H+ secretion on the cell membrane potential (V m) was tested applying pH-sensitive and conventional microelectrodes in giant cells fused from single epithelial cells of the diluting segment and in intact tubules of the frog kidney. An increase of extracellular K+ concentration from 3 to 15 mmol/l decreasedV m from −49±4 to −29±1 mV while pHi increased from 7.44±0.04 to 7.61±0.06. Addition of 1 mmol/l Ba2+ depolarizedV m from −45±3 to −32±2 mV, paralleled by an increase of pHi from 7.46±0.04 to 7.58±0.03. Application of 0.05 mmol/l furosemide hyperpolarizedV m from −48±3 to −53±3 mV and decreased pHi from 7.47±0.05 to 7.42±0.05. In the intact diluting segment of the isolated-perfused frog kidney an increase of peritubular K+ concentration from 3 to 15 mmol/l increased the luminal pH from 7.23±0.08 to 7.41±0.08. Addition of Ba2+ to the peritubular perfusate also increased luminal pH from 7.35±0.07 to 7.46±0.07. Addition of furosemide decreased luminal pH from 7.32±0.03 to 7.24±0.05. We conclude: cell depolarization reduces the driving force for the rheogenic HCO 3 − exit step across the basolateral cell membrane. HCO 3 − accumulates in the cytoplasm and pHi increases. An alkaline pHi inactivates the luminal Na+/H+ exchanger. This diminishes transepithelial H+ secretion. Cell hyperpolarization leads to the opposite phenomenon. Thus, pHi serves as signal transducer between cell voltage and Na+/H+ exchange.