GIANT VACUOLES ARISING DURING ADH-INDUCED TRANSCELLULAR BULK WATER FLOW ACROSS THE EPITHELIUM OF THE FROG URINARY BLADDER

2002 ◽  
Vol 26 (10) ◽  
pp. 873-883 ◽  
Author(s):  
Y Komissarchik
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Bulk Water ◽  
Frog Urinary Bladder

Polyclonal antibodies in study of ADH-induced water channels in frog urinary bladder

1991 ◽  
Vol 261 (3) ◽  
pp. F437-F442
Author(s):  
G. Valenti ◽  
G. Calamita ◽  
M. Svelto
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Apical Membrane ◽  
Polyclonal Antibodies ◽  
Immune Serum ◽  
Frog Urinary Bladder ◽  
Hormonal Stimulation ◽  
Osmotic Water ◽  
Triton X ◽  
Osmotic Water Flow

It is now generally accepted that changes in water permeability in anti-diuretic hormone (ADH)-responsive target epithelial cells result from the insertion in the plasma apical membrane of new components that contain channels for water. The specificity of these channels suggests that they are formed by intrinsic proteins having access to both facies and spanning the whole membrane. We have previously shown that Triton X-100 apical extracts from ADH-stimulated frog urinary bladder contain some proteins inserted under hormonal stimulation. In the present study we have developed polyclonal antibodies using Triton X-100 extract as an immunogen. After considering the inhibitory effect exerted by the whole immune serum on the osmotic water flow, we used different adsorption steps to select, from the immune serum, antibodies to apical membrane proteins inserted in response to the hormone. Immunoblot analysis of these selected antibodies shows that they recognize seven to eight proteins, of which 55-, 35-, 26-, and 17-kDa proteins are always present. Antibodies to these four proteins, affinity purified on nitrocellulose sheets, inhibited ADH-induced osmotic water flow. Altogether these results strongly suggest that proteins of 55, 35, 26, and 17 kDa (or at least one of them) are likely to be involved in the mechanism of water transport.

THE SWELLING OF FROG BLADDER CELLS PRODUCED BY OXYTOCIN

1965 ◽  
Vol 33 (2) ◽  
pp. 171-177 ◽  
Author(s):  
J. V. NATOCHIN ◽  
K. JANÁČEK ◽  
R. RYBOVÁ
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Osmotic Gradient ◽  
Frog Urinary Bladder ◽  
Intracellular Space ◽  
Osmotic Water ◽  
Inulin Space ◽  
Bladder Cells ◽  
Synthetic Oxytocin ◽  
Osmotic Water Flow

SUMMARY (1) Synthetic oxytocin (100 m-u./ml.) produces swelling of the isolated frog urinary bladder even in the absence of an osmotic gradient across the bladder. (2) Calculations show that the change in intracellular space does not necessarily differ significantly from that in the presence of an osmotic gradient since the inulin space is markedly affected by the osmotic water flow. (3) Part of the cellular potassium is exchanged for sodium during the swelling produced by oxytocin. (4) A possible mechanism and the significance of the swelling is discussed.

Wheat germ agglutinin (WGA) reduces ADH-induced water flow and induces cell surface changes in epithelial cells of frog urinary bladder

1989 ◽  
Vol 67 (2) ◽  
pp. 103-114
Author(s):  
Pierre Favard ◽  
Nina Favard ◽  
Qian Long Zhu ◽  
Jacques Bourguet ◽  
Jean-Pierre Lechaire ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Urinary Bladder ◽  
Cell Surface ◽  
Water Flow ◽  
Wheat Germ Agglutinin ◽  
Wheat Germ ◽  
Frog Urinary Bladder ◽  
Cell Surface Changes ◽  
Surface Changes

Effect of verapamil on cytoplasmic distribution of granules and microfilaments in amphibian urinary bladder

1988 ◽  
Vol 46 ◽  
pp. 324-325
Author(s):  
A.J. Mia ◽  
L.X. Oakford ◽  
T. Yorio
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Morphological Changes ◽  
Granular Cell ◽  
Cytosolic Calcium ◽  
Calcium Storage ◽  
Amphibian Urinary Bladder ◽  
Vesicular Membrane ◽  
High Concentrations ◽  
Cytoskeletal System

The amphibian urinary bladder has been used as a ‘model’ system for studies of the mechanism of action of antidiuretic hormone (ADH) in stimulating transepithelial water flow. The increase in water permeability is accompanied by morphological changes that include the stimulation of apical microvilli, mobilization of microtubules and microfilaments and vesicular membrane fusion events . It has been shown that alterations in the cytosolic calcium concentrations can inhibit ADH transmembrane water flow and induce alterations in the epithelial cell cytomorphology, including the cytoskeletal system . Recently, the subapical granules of the granular cell in the amphibian urinary bladder have been shown to contain high concentrations of calcium, and it was suggested that these cytoplasmic constituents may act as calcium storage sites for intracellular calcium homeostasis. The present study utilizes the calcium antagonist, verapamil, to examine the effect of calcium deprivation on the cytomorphological features of epithelial cells from amphibian urinary bladder, with particular emphasis on subapical granule and microfilament distribution.

A method of isolation of apical membranous sheets from frog urinary bladder epithelium by stripping with gelatin

1989 ◽  
Vol 66 (1-2) ◽  
pp. 99-106
Author(s):  
Pierre Favard ◽  
Nina Favard ◽  
Qian Long Zhu ◽  
Jacques Bourguet ◽  
Jean-Pierre Lechaire
Keyword(s):  
Urinary Bladder ◽  
Frog Urinary Bladder ◽  
Bladder Epithelium

ADH-induced water permeability and particle aggregates: alteration by a synthetic estrogen

1991 ◽  
Vol 261 (1) ◽  
pp. F144-F152 ◽  
Author(s):  
G. Calamita ◽  
Y. Le Guevel ◽  
J. Bourguet
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Water Permeability ◽  
Glucose Transporter ◽  
Apical Membrane ◽  
Selective Inhibition ◽  
Synthetic Estrogen ◽  
Permeability Changes ◽  
Particle Aggregates ◽  
Amphibian Urinary Bladder

In the amphibian urinary bladder, the increase in water permeability induced by antidiuretic hormone (ADH) is accompanied by the appearance of apical intramembrane particle (IMP) aggregates that are believed to contain specific channels for water. In a previous work, we have shown that 3,3'-diallyldiethylstilbestrol (DADES), a synthetic estrogen which is a blocker of the glucose transporter, also inhibits the hydrosmotic response to ADH in the bladder. Our aim in the present study was to analyze the alterations of the membrane fine structure further and to correlate them with the water permeability changes. The results point to a selective inhibition of the ADH-induced net water flow, probably due to an interference with one of the last steps of the response to the hormone. This inhibition is associated with an increase in the density of the apical IMP aggregates, which are thus probably not operational. The resting net water flow is not inhibited and, surprisingly, typical IMP aggregates are frequently observed in the apical membrane after DADES treatment. The compound also induces the appearance of unusual loose IMP clusters that can only be seen on the apical membrane of the granular cells and that share several ultrastructural similarities with the ADH-induced aggregates. These results suggest that 1) apical DADES treatment stimulates the insertion of IMP aggregates in the apical membrane of the urinary bladder and 2) DADES inhibits the ADH-induced water flow by interfering with the aggregates and thus probably by blocking the specific water channels.

Acidification of vasopressin-induced endosomes in toad urinary bladder

1994 ◽  
Vol 267 (1) ◽  
pp. F106-F113
Author(s):  
F. Emma ◽  
H. W. Harris ◽  
K. Strange
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Apical Membrane ◽  
Fluid Phase ◽  
Endocytic Pathway ◽  
Toad Urinary Bladder ◽  
Acidic Ph ◽  
Terminal Event ◽  
Ultimate Fate

It is well established that water channels (WC) are removed from the apical membrane of vasopressin-sensitive epithelia by endocytosis. The processing and the ultimate fate of endocytosed WC is, however, incompletely understood. In many cells, endosome acidification plays an important role in the processing and sorting of endocytosed proteins. Endosome acidification in the toad urinary bladder was therefore examined in vivo by fluorescence ratio video microscopy after induction of endocytosis by vasopressin removal and transepithelial water flow in the presence of the pH-sensitive fluid phase marker 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-dextran. Fifteen minutes after induction of endocytosis, the majority of endosomes had a neutral or slightly acidic pH. The number of acidic endosomes increased progressively with time. Two hours after endocytosis began, 98% of the endosomes had a pH < 6.0. Bafilomycin completely blocked endosome acidification, indicating that H+ transport is mediated by a vacuolar H(+)-adenosinetriphosphatase. Bafilomycin had no effect on transepithelial water flow in bladders repetitively stimulated by vasopressin. These findings, as well as the work of other investigators, suggest that if WC recycling occurs, it is not dependent on acidification of the endosomal compartment. Acidification of vasopressin-induced endosomes most likely represents a terminal event in the endocytic pathway.

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