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Bladder Epithelium

The Experts below are selected from a list of 141 Experts worldwide ranked by ideXlab platform

Douglas R Ferguson – 1st expert on this subject based on the ideXlab platform

  • regulation of na channel density at the apical surface of rabbit urinary Bladder Epithelium
    European Journal of Pharmacology, 2002
    Co-Authors: Timothy J Burton, Michael J Edwardson, Jamie Ingham, Heidi V Tempest, Douglas R Ferguson

    Abstract:

    Abstract We have investigated the effects of various manipulations on Na+ transport across the rabbit urinary Bladder Epithelium. After Bladders were mounted in Ussing chambers there was a spontaneous and significant (>4-fold) increase in amiloride-sensitive short-circuit current (equivalent to net Na+ transport) over a 6-h period. The increase in current was almost abolished by brefeldin A, an inhibitor of anterograde vesicular transport, and reduced after a 3-h delay by cycloheximide, an inhibitor of protein synthesis. The spontaneous increase in short-circuit current was potentiated by treatment of Bladders with either forskolin, which causes an elevation in cAMP levels, or aldosterone. Acting together, these two agents produced a significant synergistic effect on short-circuit current. The short-circuit current recovered rapidly after reduction in intracellular Na+ levels, achieved either by lowering the extracellular Na+ concentration or blockade of epithelial Na+ channels with the sulphydryl modifying reagent p-chloromercuribenzenesulphonic acid (PCMBS). Recovery after PCMBS treatment was partially sensitive to brefeldin A. Short-circuit current saturated as the extracellular Na+ concentration was increased (EC50=51 mM). Saturation occurred over a range of Na+ concentrations in which single channel permeability is known to remain constant, indicating that it depends on a reduction in epithelial Na+ channel density at the apical plasma membrane. Exposure of Bladders to a high Na+ concentration caused an increase in endocytotic activity, detected through an increase in the uptake of the fluid-phase marker fluorescein isothiocyanate (FITC)–dextran into vesicles located beneath the apical plasma membrane. We conclude that the urinary Bladder Epithelium is able to respond rapidly and efficiently to changes in its environment by regulating the density of epithelial Na+ channels in its apical surface.

  • Regulation of Na+ channel density at the apical surface of rabbit urinary Bladder Epithelium.
    European journal of pharmacology, 2002
    Co-Authors: Timothy J Burton, Jamie Ingham, Heidi V Tempest, J Michael Edwardson, Douglas R Ferguson

    Abstract:

    We have investigated the effects of various manipulations on Na(+) transport across the rabbit urinary Bladder Epithelium. After Bladders were mounted in Ussing chambers there was a spontaneous and significant (>4-fold) increase in amiloride-sensitive short-circuit current (equivalent to net Na(+) transport) over a 6-h period. The increase in current was almost abolished by brefeldin A, an inhibitor of anterograde vesicular transport, and reduced after a 3-h delay by cycloheximide, an inhibitor of protein synthesis. The spontaneous increase in short-circuit current was potentiated by treatment of Bladders with either forskolin, which causes an elevation in cAMP levels, or aldosterone. Acting together, these two agents produced a significant synergistic effect on short-circuit current. The short-circuit current recovered rapidly after reduction in intracellular Na(+) levels, achieved either by lowering the extracellular Na(+) concentration or blockade of epithelial Na(+) channels with the sulphydryl modifying reagent p-chloromercuribenzenesulphonic acid (PCMBS). Recovery after PCMBS treatment was partially sensitive to brefeldin A. Short-circuit current saturated as the extracellular Na(+) concentration was increased (EC(50) = 51 mM). Saturation occurred over a range of Na(+) concentrations in which single channel permeability is known to remain constant, indicating that it depends on a reduction in epithelial Na(+) channel density at the apical plasma membrane. Exposure of Bladders to a high Na(+) concentration caused an increase in endocytotic activity, detected through an increase in the uptake of the fluid-phase marker fluorescein isothiocyanate (FITC)-dextran into vesicles located beneath the apical plasma membrane. We conclude that the urinary Bladder Epithelium is able to respond rapidly and efficiently to changes in its environment by regulating the density of epithelial Na(+) channels in its apical surface.

John W Hanrahan – 2nd expert on this subject based on the ideXlab platform

  • physiological approaches for studying mammalian urinary Bladder Epithelium
    Methods in Enzymology, 1990
    Co-Authors: Simon A Lewis, John W Hanrahan

    Abstract:

    Publisher Summary This chapter describes the methods used to measure the physiological properties of the mammalian urinary Bladder Epithelium in vitro . This involves the selection of a bathing solution similar in composition to plasma, development of a method to remove the muscle layers from the Epithelium with minimal traumatization of the tissue, design of an in vitro chamber into which the Epithelium is mounted with minimal damage, and choice of an electrical recording system to assess the transepithelial properties of the tissues in a nonintrusive manner. This chapter also discusses methods that were used during this work, emphasizing modifications that are unique to this particular tissue. The mammalian urinary Bladder offers many advantages over other Na + -transporting epithelia that are widely used as model preparations. The apical cell layer seems not to be coupled to the lower two germinal cell layers, and this apical layer is composed of only one cell type.

Timothy J Burton – 3rd expert on this subject based on the ideXlab platform

  • regulation of na channel density at the apical surface of rabbit urinary Bladder Epithelium
    European Journal of Pharmacology, 2002
    Co-Authors: Timothy J Burton, Michael J Edwardson, Jamie Ingham, Heidi V Tempest, Douglas R Ferguson

    Abstract:

    Abstract We have investigated the effects of various manipulations on Na+ transport across the rabbit urinary Bladder Epithelium. After Bladders were mounted in Ussing chambers there was a spontaneous and significant (>4-fold) increase in amiloride-sensitive short-circuit current (equivalent to net Na+ transport) over a 6-h period. The increase in current was almost abolished by brefeldin A, an inhibitor of anterograde vesicular transport, and reduced after a 3-h delay by cycloheximide, an inhibitor of protein synthesis. The spontaneous increase in short-circuit current was potentiated by treatment of Bladders with either forskolin, which causes an elevation in cAMP levels, or aldosterone. Acting together, these two agents produced a significant synergistic effect on short-circuit current. The short-circuit current recovered rapidly after reduction in intracellular Na+ levels, achieved either by lowering the extracellular Na+ concentration or blockade of epithelial Na+ channels with the sulphydryl modifying reagent p-chloromercuribenzenesulphonic acid (PCMBS). Recovery after PCMBS treatment was partially sensitive to brefeldin A. Short-circuit current saturated as the extracellular Na+ concentration was increased (EC50=51 mM). Saturation occurred over a range of Na+ concentrations in which single channel permeability is known to remain constant, indicating that it depends on a reduction in epithelial Na+ channel density at the apical plasma membrane. Exposure of Bladders to a high Na+ concentration caused an increase in endocytotic activity, detected through an increase in the uptake of the fluid-phase marker fluorescein isothiocyanate (FITC)–dextran into vesicles located beneath the apical plasma membrane. We conclude that the urinary Bladder Epithelium is able to respond rapidly and efficiently to changes in its environment by regulating the density of epithelial Na+ channels in its apical surface.

  • Regulation of Na+ channel density at the apical surface of rabbit urinary Bladder Epithelium.
    European journal of pharmacology, 2002
    Co-Authors: Timothy J Burton, Jamie Ingham, Heidi V Tempest, J Michael Edwardson, Douglas R Ferguson

    Abstract:

    We have investigated the effects of various manipulations on Na(+) transport across the rabbit urinary Bladder Epithelium. After Bladders were mounted in Ussing chambers there was a spontaneous and significant (>4-fold) increase in amiloride-sensitive short-circuit current (equivalent to net Na(+) transport) over a 6-h period. The increase in current was almost abolished by brefeldin A, an inhibitor of anterograde vesicular transport, and reduced after a 3-h delay by cycloheximide, an inhibitor of protein synthesis. The spontaneous increase in short-circuit current was potentiated by treatment of Bladders with either forskolin, which causes an elevation in cAMP levels, or aldosterone. Acting together, these two agents produced a significant synergistic effect on short-circuit current. The short-circuit current recovered rapidly after reduction in intracellular Na(+) levels, achieved either by lowering the extracellular Na(+) concentration or blockade of epithelial Na(+) channels with the sulphydryl modifying reagent p-chloromercuribenzenesulphonic acid (PCMBS). Recovery after PCMBS treatment was partially sensitive to brefeldin A. Short-circuit current saturated as the extracellular Na(+) concentration was increased (EC(50) = 51 mM). Saturation occurred over a range of Na(+) concentrations in which single channel permeability is known to remain constant, indicating that it depends on a reduction in epithelial Na(+) channel density at the apical plasma membrane. Exposure of Bladders to a high Na(+) concentration caused an increase in endocytotic activity, detected through an increase in the uptake of the fluid-phase marker fluorescein isothiocyanate (FITC)-dextran into vesicles located beneath the apical plasma membrane. We conclude that the urinary Bladder Epithelium is able to respond rapidly and efficiently to changes in its environment by regulating the density of epithelial Na(+) channels in its apical surface.