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  • 1
    ISSN: 1432-2013
    Keywords: Diluting segment ; Cell fusion ; Intracellular pH ; Cell membrane potential ; Frog kidney
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 408 (1987), S. 291-299 
    ISSN: 1432-2013
    Keywords: Diluting segment ; Cell fusion ; Na+/HCO 3 − ; Cotransport ; SITS ; Acetazolamide ; Frog kidney
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanism of HCO 3 − transport was studied applying microelectrodes in “giant” cells fused from single epithelial cells of the diluting segment of frog kidney. A sudeen increase of extracellular HCO 3 − concentration from 10 to 20 mmol/l at constant pH hyperpolarized the cell membrane potential of the fused cell. This cell-voltage response was totally abolished by 10−3 mol/l SITS and significantly reduced by 10−4 mol/l acetazolamide or by omission of Na+ from the extracellular perfusate. Removal of Na+ from the perfusate caused a transient depolarization. Reapplication of Na+ induced a transient hyperpolarization. 10−3 mol/l SITS abolished the cell-voltage response to removal and reapplication of Na+. In the intact diluting segment of the isolated perfused frog kidney peritubular perfusion of 10−4 mol/l acetazolamide reduced the limiting transepithelial electrochemical gradient for H+ significantly from 30±4 mV to 14±3 mV. The results suggest: (i) In the diluting segment of the frog kidney a Na+-dependent rheogenic HCO 3 − transport system exists across the peritubular cell membrane. (ii) This rheogenic peritubular Na+/HCO 3 − cotransporter cooperates with a Na+/H+ exchanger in the luminal membrane, thus driving HCO 3 − reabsorption. (iii) Reabsorption of HCO 3 − and secretion of H+ depend upon the presence of carbonic anhydrase.
    Type of Medium: Electronic Resource
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