Water Permeability of Amphibian Urinary Bladder

2018 ◽  
pp. 169-196
Author(s):  
Jacques Bourguet ◽  
Jacques Chevalier ◽  
Mario Parisi ◽  
Pierre Ripoche
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Amphibian Urinary Bladder

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.

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.

Progesterone inhibition of water permeability in Bufo arenarum oocytes and urinary bladder

1996 ◽  
Vol 270 (5) ◽  
pp. F880-F885 ◽  
Author(s):  
P. Ford ◽  
G. Amodeo ◽  
C. Capurro ◽  
C. Ibarra ◽  
R. Dorr ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Xenopus Laevis ◽  
Water Permeability ◽  
Water Channel ◽  
Water Channels ◽  
Toad Urinary Bladder ◽  
Osmotic Permeability ◽  
Bufo Arenarum ◽  
Mrna Extraction

The ovarian oocytes from Bufo arenarum (BAO) but not those from Xenopus laevis (XLO) would have water channels (WC). We now report that the injection of the mRNA from BAO into the oocytes from XLO increased their water osmotic permeability (Pi) (reduced by 0.3 mM HgCl2 and reversed by 5 mM beta-mercaptoethanol). A 30-min challenge with progesterone induced, 18 h later, a reduction of the mercury-sensitive fraction of Pf in the BAO (but not in XLO). The mRNA from BAO pretreated with progesterone lost its capacity to induce WC in the XLO, but the hormone did not affect the expression of the WC in XLO previously injected with the mRNA from BAO. Pf was also measured in urinary bladders of BAO. Eighteen hours after a challenge with progesterone, a reduction in the hydrosmotic response to oxytocin was observed. Finally, the mRNA from the urinary bladder of BAO was injected into XLO. An increase in Pf was observed. This was not the case if, before the mRNA extraction, the bladders were treated with progesterone. We conclude that the BAO WC share progesterone sensitivity with the oxytocin-regulated water channel present in the toad urinary bladder.

Vasopressin-elicited refractoriness of the response to vasopressin in toad urinary bladder

1981 ◽  
Vol 240 (6) ◽  
pp. F551-F557 ◽  
Author(s):  
J. S. Handler ◽  
A. S. Preston
Keyword(s):  
Urinary Bladder ◽  
Adenylate Cyclase ◽  
Water Permeability ◽  
Recovery Period ◽  
Ringer Solution ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Toad Urinary Bladder ◽  
Camp Phosphodiesterase ◽  
Prolonged Incubation

Incubation of the urinary bladder of Bufo marinus with high concentrations of vasopressin produces refractoriness to subsequent stimulation of water permeability by low concentrations of vasopressin. Development of refractoriness is directly dependent on concentration of vasopressin and duration of incubation with the hormone. Refractoriness develops in the absence of transepithelial water flow, is evident following a 2-h recovery period of incubation in hormone-free Ringer solution, and is reversed after prolonged incubation in hormone-free Ringer solution. Development and reversal of refractoriness is not altered by actinomycin D or cycloheximide. The steps at which refractoriness develops have been identified partially. Under different conditions, refractoriness involves: 1) reduced vasopressin-sensitive adenylate cyclase activity, 2) reduced epithelial cell cAMP accumulation in response to vasopressin the absence of demonstrable change in vasopressin-sensitive adenylate cyclase activity, cAMP phosphodiesterase activity, or loss of cAMP into the Ringer solution, and 3) refractoriness of water permeability response to exogenous cAMP.

Activation of actin-containing microfilaments by vasopressin in the amphibian urinary bladder epithelium: A fluorescent study using NBD-phallacidin

1985 ◽  
Vol 211 (3) ◽  
pp. 239-245 ◽  
Author(s):  
Walter L. Davis ◽  
Ruth Gwendolyn Jones ◽  
Phillip C. Richemont ◽  
David B. P. Goodman
Keyword(s):  
Urinary Bladder ◽  
Bladder Epithelium ◽  
Amphibian Urinary Bladder

Antidiuretic hormone-induced intramembranous alterations in mammalian collecting ducts

1978 ◽  
Vol 235 (5) ◽  
pp. F440-F443 ◽  
Author(s):  
Mehmet C. Harmanci ◽  
William A. Kachadorian ◽  
Heinz Valtin ◽  
Vincent A. DiScala
Keyword(s):  
Urinary Bladder ◽  
Antidiuretic Hormone ◽  
Collecting Duct ◽  
Freeze Fracture ◽  
Intramembranous Particle ◽  
Membrane Effect ◽  
Collecting Ducts ◽  
Amphibian Urinary Bladder ◽  
Freeze Fracture Electron Microscopy ◽  
Membrane Particle

Freeze-fracture electron microscopy had previously revealed antidiuretic hormone-induced aggregates of intramembranous particles in amphibian urinary bladder. To investigate the effects of antidiuretic hormone (ADH) in another ADH-sensitive epithelium, namely, mammalian renal collecting ducts, freeze-fracture studies were carried out in Brattleboro homozygous rats. Collecting duct luminal membranes of ADH-treated homozygotes showed intramembranous particle clusters (117 ± 17/100 μm2) that were loosely packed and that occurred on both exoplasmic (E) and protoplasmic (P) faces. Untreated, control homozygous rats had significantly less (3 ± 1/100 μm2) clusters. Changes similar to those seen in ADH-treated rats were observed in water-deprived Wistar rats. The clustered particles differed from those seen in ADH-treated amphibian urinary bladder in that the latter occurred only on the P face and were more densely packed. Nevertheless, our observations suggest a common membrane effect for ADH action that may apply in mammals and amphibia alike. freeze-fracture; Brattleboro homozygous rats; membrane particle clusters Submitted on March 6, 1978 Accepted on July 14, 1978

Release of cyclic AMP by toad urinary bladder

1975 ◽  
Vol 228 (3) ◽  
pp. 954-958 ◽  
Author(s):  
S Urakabe ◽  
JS Handler ◽  
J Orloff
Keyword(s):  
Epithelial Cells ◽  
Urinary Bladder ◽  
Cyclic Amp ◽  
Cell Membrane ◽  
Water Permeability ◽  
Ringer Solution ◽  
Mucosal Surface ◽  
Toad Urinary Bladder ◽  
Solution Bathing

Cyclic AMP accumulates in the Ringer solution bathing the toad urinary bladder in vitro. At least 4 times more cyclic AMP is released into the solution bathing the serosal surface than into the solution bathing the mucosal surface. Most of the cyclic AMP originates in the epithelial cells rather than the stroma. Vasopressin increased the content of cyclic AMP in the epithelial cells and increases the amount of cyclic AMP in the Ringer solution. Since there is not an increase in medium cyclic AMP when cell cyclic AMP levels are increased by theophylline, it is suggested that theophylline may reduce the permeability of the cell membrane to cyclic AMP. Finally, it is demonstrated that 10 mM NaF increase the amount of cyclic AMP in the epithelial cells and in the solution bathing the bladder, but block the effect of vasopressin on water permeability, presumably at a step subsequent to the formation of cyclic AMP.

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