Apical and basolateral membrane ionic channels in rabbit urinary bladder epithelium

1985 ◽  
Vol 405 (S1) ◽  
pp. S83-S88 ◽  
Author(s):  
Simon A. Lewis ◽  
John W. Hanrahan
Keyword(s):  
Urinary Bladder ◽  
Basolateral Membrane ◽  
Ionic Channels ◽  
Bladder Epithelium ◽  
Rabbit Urinary Bladder

scholarly journals Anion-sensitive sodium conductance in the apical membrane of toad urinary bladder.

1980 ◽  
Vol 76 (1) ◽  
pp. 69-81 ◽  
Author(s):  
J Narvarte ◽  
A L Finn
Keyword(s):  
Membrane Potential ◽  
Urinary Bladder ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Membrane Potentials ◽  
Toad Urinary Bladder ◽  
Bladder Epithelium ◽  
Anionic Composition ◽  
Before And After ◽  
Cl Conductance

Membrane potentials and the electrical resistance of the cell membranes and the shunt pathway of toad urinary bladder epithelium were measured using microelectrode techniques. These measurements were used to compute the equivalent electromotive forces (EMF) at both cell borders before and after reductions in mucosal Cl- concentration ([Cl]m). The effects of reduction in [Cl]m depended on the anionic substitute. Gluconate or sulfate substitutions increased transepithelial resistance, depolarized membrane potentials and EMF at both cell borders, and decreased cell conductance. Iodide substitutions had opposite effects. Gluconate or sulfate substitutions decreased apical Na conductance, where iodide replacements increased it. When gluconate or sulfate substitutions were brought about the presence of amiloride in the mucosal solution, apical membrane potential and EMF hyperpolarized with no significant changes in basolateral membrane potential or EMF. It is concluded that: (a) apical Na conductance depends, in part, on the anionic composition of the mucosal solution, (b) there is a Cl- conductance in the apical membrane, and (c) the electrical communication between apical and basolateral membranes previously described is mediated by changes in the size of the cell Na pool, most likely by a change in sodium activity.

Site-specific regulation of organic osmolytes along the rat nephron

1996 ◽  
Vol 271 (3) ◽  
pp. F645-F652 ◽  
Author(s):  
M. Schmolke ◽  
A. Bornemann ◽  
W. G. Guder
Keyword(s):  
Urinary Bladder ◽  
High Performance ◽  
Lithium Treatment ◽  
Basolateral Membrane ◽  
Organic Osmolytes ◽  
Bladder Epithelium ◽  
Site Specific ◽  
Urinary Osmolality ◽  
Specific Regulation ◽  
Microdissected Tubules

The regulation of organic osmolytes was investigated in acute furosemide and chronic lithium diuresis along the nephron and in urinary bladder of rats. Sorbitol, myo-inositol, glycerophosphorylcholine, and betaine were measured enzymatically or by high performance liquid chromatography in homogenates and bioluminometrically in microdissected tubules. In untreated rats, all osmolytes except myo-inositol increased along the corticopapillary axis. An efflux of all osmolytes (-50%) was observed in homogenates of outer and inner medulla after acute furosemide diuresis (15 min, urinary osmolality = 329 mosmol/kgH2O) and for both polyols in microdissected tubules (30 min). In urinary bladder, only low concentrations of myo-inositol were found not to be affected by furosemide treatment. Chronic lithium treatment (7 days; urinary osmolality = 385 mosmol/kgH2O) decreased inner medullary but not outer medullary osmolyte concentrations. The results confirm a site-specific organic osmolyte pattern along the rat nephron, which is rapidly changed in a segment-specific way by different mechanisms of diuresis. The bladder epithelium does not accumulate organic osmolytes because no "osmotic gap" exists across the basolateral membrane. The osmotic difference across the apical membrane is maintained by the apical tightness of these cells.

Effect of hyperosmotic challenge on basolateral membrane potential in rabbit urinary bladder

1990 ◽  
Vol 258 (2) ◽  
pp. C248-C257 ◽  
Author(s):  
P. J. Donaldson ◽  
S. A. Lewis
Keyword(s):  
Membrane Potential ◽  
Urinary Bladder ◽  
Basolateral Membrane ◽  
Pump Current ◽  
Bathing Solution ◽  
Partial Recovery ◽  
Parallel Operation ◽  
Voltage Recovery ◽  
Rabbit Urinary Bladder ◽  
Basolateral Membrane Potential

In the rabbit urinary bladder, serosal hyperosmotic challenge (SHOC) with either 33 mM NaCl or 66 mM mannitol caused basolateral membrane potential (Vbl) to initially depolarize from -52.6 +/- 1.6 to -48.4 +/- 1.4 mV, followed by a recovery of Vbl to -57.5 +/- 1.3 mV after 13.7 +/- 1.0 min. The voltage recovery was dependent on both serosal HCO3- and Cl-, and in the absence of both, Vbl depolarized to -11.6 +/- 1.5 mV and the ratio of apical-to-basolateral resistance (Ra/Rbl) decreased from 21.0 +/- 3.4 to 8.3 +/- 3.1. This decrease in Ra/Rbl and consequent depolarization of Vbl is caused by a decrease in basolateral K+ conductance. Replacement of serosal Cl- with NO3- or SCN- followed by SHOC caused a sustained depolarization of Vbl to -32.5 +/- 4.4 and -40.9 +/- 0.9 mV, respectively. However, when Br- was used to replace Cl-, voltage recovery occurred but was slowed (24.0 +/- 2.7 min) and reduced in magnitude (-47.5 +/- 3.5 mV). Addition of amiloride (1 mM) or niflumic acid (100 microM), but not bumetanide (1 microM), to the serosal bathing solution inhibited voltage recovery causing Vbl to depolarize to -36.3 +/- 2.6 and -41.5 +/- 4.5 mV, respectively. Serosal addition of ouabain after SHOC caused Vbl to depolarize by 10.8 +/- 0.9 mV in 2 min. We speculate that the SHOC-induced initial depolarization of Vbl is a loss of Ba2(+)-sensitive K+ conductance caused by cell shrinkage. The subsequent repolarization/hyperpolarization of Vbl is caused by an enhanced basolateral membrane Na+ pump current and a reappearance of the Ba2(+)-sensitive K+ conductance. The parallel operation of Na(+)-H+ and Cl(-)-HCO3- exchanges will then supply Na+ for the pump current and, via cellular accumulation of Na+, K+, and Cl-, might result in a partial recovery of cell volume and thus Ba2(+)-sensitive K+ conductance.

Active and passive Na+ fluxes across the basolateral membrane of rabbit urinary bladder

1982 ◽  
Vol 67 (1) ◽  
pp. 219-229 ◽  
Author(s):  
Douglas C. Eaton ◽  
A. Michael Frace ◽  
S. Unglaub Silverthorn
Keyword(s):  
Urinary Bladder ◽  
Basolateral Membrane ◽  
Rabbit Urinary Bladder

scholarly journals Sodium transport effects on the basolateral membrane in toad urinary bladder.

1982 ◽  
Vol 80 (5) ◽  
pp. 733-751 ◽  
Author(s):  
C W Davis ◽  
A L Finn
Keyword(s):  
Urinary Bladder ◽  
Time Course ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Membrane Resistance ◽  
Membrane Voltage ◽  
Toad Urinary Bladder ◽  
Na Transport ◽  
Bladder Epithelium ◽  
Current Output

In toad urinary bladder epithelium, inhibition of Na transport with amiloride causes a decrease in the apical (Vmc) and basolateral (Vcs) membrane potentials. In addition to increasing apical membrane resistance (Ra), amiloride also causes an increase in basolateral membrane resistance (Rb), with a time course such that Ra/Rb does not change for 1-2 min. At longer times after amiloride (3-4 min), Ra/Rb rises from its control values to its amiloride steady state values through a secondary decrease in Rb. Analysis of an equivalent electrical circuit of the epithelium shows that the depolarization of Vcs is due to a decrease in basolateral electromotive force (Vb). To see of the changes in Vcs and Rb are correlated with a decrease in Na transport, external current (Ie) was used to clamp Vmc to zero, and the effects of amiloride on the portion of Ie that takes the transcellular pathway were determined. In these studies, Vcs also depolarized, which suggests that the decrease in Vb was due to a decrease in the current output of a rheogenic Na pump. Thus, the basolateral membrane does not behave like an ohmic resistor. In contrast, when transport is inhibited during basolateral membrane voltage clamping, the apical membrane voltage changes are those predicted for a simple, passive (i.e., ohmic) element.

Effects of serosal anion composition on the permeability properties of rabbit urinary bladder

1989 ◽  
Vol 256 (6) ◽  
pp. F1125-F1134
Author(s):  
P. J. Donaldson ◽  
L. K. Chen ◽  
S. A. Lewis
Keyword(s):  
Urinary Bladder ◽  
Basolateral Membrane ◽  
Anion Channel ◽  
Membrane Properties ◽  
Lag Phase ◽  
Na Transport ◽  
Transepithelial Na Transport ◽  
Bladder Replacement ◽  
Lag Period ◽  
Rabbit Urinary Bladder

This study describes the effects of serosal Cl- and HCO3- substitution on transepithelial Na+ transport and basolateral membrane properties of the rabbit urinary bladder. Replacement of Cl- with NO3-, SCN-, and Br- had no effect on transepithelial Na+ transport or the basolateral membrane potential (Vbl). However, gluconate, isethionate, and cyclamate (anions that were shown previously to be not as permeable as Cl- through the basolateral membrane anion channel), decreased transepithelial Na+ transport and depolarized Vbl. Replacement of HCO3- also produced a decrease in transepithelial Na+ transport and a depolarization of Vbl. Utilizing conventional and K+-specific microelectrodes, we found the depolarization to be due to a reduction in basolateral K+ conductance. This depolarization was reversible only when Cl- was returned to the serosal solution, the normally permeant anion NO3- being unable to affect repolarization, suggesting that both the K+ and Cl- conductance are reduced during depolarization. A lag period of some 4 min preceded the repolarization of Vbl. The Na+-H+ exchange blocker amiloride prolonged the lag phase associated with repolarization, whereas niflumic acid, a Cl-(-)HCO3- exchange blocker (in red blood cells) reduced the magnitude of Vbl repolarization. Because of the possible involvement of the exchangers it is believed that the lag phase represents a volume-dependent and/or pH-dependent reactivation of the basolateral membrane conductances.

Regulation of Na+ channel density at the apical surface of rabbit urinary bladder epithelium

2002 ◽  
Vol 448 (2-3) ◽  
pp. 215-223 ◽  
Author(s):  
Timothy J Burton ◽  
J.Michael Edwardson ◽  
Jamie Ingham ◽  
Heidi V Tempest ◽  
Douglas R Ferguson
Keyword(s):  
Urinary Bladder ◽  
Na Channel ◽  
Apical Surface ◽  
Bladder Epithelium ◽  
Channel Density ◽  
Rabbit Urinary Bladder

Initial effects of cyclophosphamide on urinary bladder epithelium in the rat

Pathology ◽  
1974 ◽  
Vol 6 (4) ◽  
pp. 343-350 ◽  
Author(s):  
Mary E. Schultz ◽  
Michael W. Weldon
Keyword(s):  
Urinary Bladder ◽  
Bladder Epithelium

Effect of Chronic Nitrofurantoin Administration on the Rabbit Urinary Bladder

1987 ◽  
Vol 137 (6) ◽  
Author(s):  
Philip M. Hanno ◽  
Beth Witkowski
Keyword(s):  
Urinary Bladder ◽  
Rabbit Urinary Bladder

Membrane associated particles: Distribution in frog urinary bladder epithelium at rest and after oxytocin treatment

1974 ◽  
Vol 152 (2) ◽  
pp. 129-140 ◽  
Author(s):  
J. Chevalier ◽  
J. Bourguet ◽  
J. S. Hugon
Keyword(s):  
Urinary Bladder ◽  
Frog Urinary Bladder ◽  
Bladder Epithelium
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