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  • Membrane potentials  (2)
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 424 (1993), S. 145-151 
    ISSN: 1432-2013
    Keywords: Rat hepatocytes ; Electrophysiology ; Membrane potentials ; Na+ conductance ; Bile acids ; Taurocholic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rat hepatocytes in primary culture were impaled with conventional microelectrodes. Addition of 5–100 μmol/l taurocholate led to a slowly developing depolarization that was maximal at 50 μmol/l (10.5±1.5 mV, n=15) and not reversible. The effect was Na+ dependent and decreased in cells preincubated with 1 μmol/l taurocholate. Increasing external K+ tenfold depolarized the cells by 12.3±2.3 mV under control conditions and by 6.3±1.2 mV with 50 μmol/l taurocholate present (n=7). Depolarization by 1 mmol/l Ba2+ was 7.6±0.8 mV and 6.0±0.7 mV (n=9) before and after addition of taurocholate, respectively. Cable analysis and Na+ substitution experiments reveal that this apparent decrease in K+ conductance reflects an actual increase in Na+ conductance: in the presence of taurocholate, specific cell membrane resistance decreased from 2.8 to 2.3 kΩ · cm2 · Na+ substitution by 95% depolarized cell membranes by 8.9±2.9 mV (n=9), probably due to indirect effects on K+ conductance via changes in cell pH. With taurocholate present, the same manoeuvre changed membrane voltages by −0.8±2.6 mV. When Na+ concentration was restored to 100% from solutions containing 5% Na+, cells hyperpolarized by 3.5±3.6 mV (n=7) under control conditions and depolarized by 4.4±2.9 mV in the presence of taurocholate, respectively. In Cl− substitution experiments, there was no evidence for changes in Cl− conductance by taurocholate. These results show that taurocholate-induced membrane depolarization is due to an increase in Na+ conductance probably via uptake of the bile acid.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2013
    Keywords: HCO3 secretion ; Membrane potentials ; Cell membrane ion permeabilities ; Ouabain ; Prostaglandin E1 ; Loperamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Loperamide inhibits PGE1-induced electrogenic HCO3 secretion in guinea-pig gallbladder. Underlying changes in epithelial cell membrane properties were investgated using intracellular microelectrode techniques in vitro. In the absence of PGE1, mucosal loperamide (10−4 mol/l) reversibly depolarized both cell membranes by ∼ 6 mV. The apparent ratio of membrane resistances (R a/R b) remained unchanged and so did voltage responses to luminal Cl removal and Na reduction. The depolarizing response to elevation of luminal K concentration from 5 to 76 mmol/l was decreased from 13 to 8 mV. In the presence of 1 PGE1, the apical membrane is mainly permeable to Cl and HCO3. Under these conditions, loperamide reduced membrane potentials by ∼ 10 mV,R a/R b remaining constant at ∼ 0.4. Effects on voltage responses to changes in luminal Na or K concentration were unchanged. Responses to luminal Cl removal (transient depolarization) were greatly enhanced (from 22 to 42 mV) as predictable from the fall in K permeability that hinders Cl efflux from cell into lumen. Less marked but significant effects were obtained with 10−5 mol/l (mucosal side) and serosal loperamide (10−4 mol/l). We suggest that loperamide inhibits electrogenic HCO3 secretion by reducing apical membrane K permeability. The resulting depolarization diminishes the driving force for conductive anion efflux from cell into lumen. This conclusion is supported by the ability of luminal K elevation to mimick loperamide inhibition of the secretory flux of HCO3 (pH-stat experiments).
    Type of Medium: Electronic Resource
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