Role of the cytoskeleton in the control of transcellular water flow by vasopressin in amphibian urinary bladder

1985 ◽  
Vol 55 (3) ◽  
pp. 163-172 ◽  
Author(s):  
M. Pearl ◽  
A. Taylor
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Amphibian Urinary Bladder

Role of PKC isozyme III (γ) in water transport in amphibian urinary bladder

1992 ◽  
Vol 50 (1) ◽  
pp. 796-797
Author(s):  
A.J Mia ◽  
L.X. Oakford ◽  
P.D. Thompson ◽  
Z.H. Ning ◽  
T. Yorio
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Phorbol Esters ◽  
Apical Membrane ◽  
Protein A ◽  
Water Channels ◽  
Renal Epithelia ◽  
Amphibian Urinary Bladder ◽  
Pkc Isozymes

Vasopressin stimulated water flow across renal epithelia is thought to occur through a V2 receptor coupled to adenylcyclase. The increase in water flow occurs as a result of a fusion of water channels with the apical membrane and is indicative of an increase in membrane capacitance following hormone addition.What controls the cycling of water channels and their insertion into the membrane is uncertain. Our laboratory has demonstrated that renal epithelia as well as amphibian urinary bladder membranes, contain a vasopressin V1 receptor which upon activation results in the breakdown of phosphoinositide and the formation of inositol triphosphate and diacylglycerol, the latter an activator of protein kinase C (PKC). The initiation of transepithelial water flow also appears to involve V1 receptors and possibly activation of PKC. To test this hypothesis, we have been using activators of PKC, such as phorbol esters and mezerein, as pharmacological tools to determine if PKC activation results in similar physiological responses as the hormone. Several PKC isozymes, upon activation, are known to be translocated to the apical membrane as visualized by FITC immunofluorescence. Previously, we reported co-localization of PKC subtypes I (γ) and II (β) in toad urinary bladders using monoclonal antibodies and protein A-gold probes. This report includes the localization of PKC subtype III (α) and its distribution pattern using immunogold labeling.

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.

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.

Water flow in the toad urinary bladder in response to vasopressin: role of potassium

1989 ◽  
Vol 66 (1-2) ◽  
pp. 43-51 ◽  
Author(s):  
Christos P. Carvounis ◽  
Georgia Carvounis ◽  
Cheryl Bernstein ◽  
Mary E. Oros
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Toad Urinary Bladder

Role of PKC isozymes in water transport in toad urinary bladder

1991 ◽  
Vol 49 ◽  
pp. 302-303
Author(s):  
A.J. Mia ◽  
L.X. Oakford ◽  
T. Yorio
Keyword(s):  
Urinary Bladder ◽  
Apical Membrane ◽  
Membrane Surface ◽  
Protein A ◽  
Cell Types ◽  
Leukemic Cells ◽  
Toad Urinary Bladder ◽  
Pkc Isozymes ◽  
Antibody Labeling

Protein kinase C (PKC) isozymes, when activated, are translocated to particulate membrane fractions for transport to the apical membrane surface in a variety of cell types. Evidence of PKC translocation was demonstrated in human megakaryoblastic leukemic cells, and in cardiac myocytes and fibroblasts, using FTTC immunofluorescent antibody labeling techniques. Recently, we reported immunogold localizations of PKC subtypes I and II in toad urinary bladder epithelia, following 60 min stimulation with Mezerein (MZ), a PKC activator, or antidiuretic hormone (ADH). Localization of isozyme subtypes I and n was carried out in separate grids using specific monoclonal antibodies with subsequent labeling with 20nm protein A-gold probes. Each PKC subtype was found to be distributed singularly and in discrete isolated patches in the cytosol as well as in the apical membrane domains. To determine if the PKC isozymes co-localized within the cell, a double immunogold labeling technique using single grids was utilized.

THE ROLE OF THE MOTHER IN 131I METABOLISM OF SUCKING AND WEANLING RATS

1965 ◽  
Vol 43 (3) ◽  
pp. 431-436 ◽  
Author(s):  
M. Samel ◽  
A. Caputa
Keyword(s):  
Urinary Bladder ◽  
In Utero ◽  
The State ◽  
Newborn Rats ◽  
Weanling Rats ◽  
Immature Rats ◽  
Other Substances ◽  
Old Rats

In newborn rats the mother provokes the emptying of the urinary bladder by stimulating the perineum with her tongue. The possibility that mothers may thereby ingest the urine of their young has been studied by means of 131I on nine litters of rats aged 10 to 29 days. The results indicate that a considerable quantity of 131I administered intraperitoneally to 10- and 18-day-old rats, which were then reunited with their mothers for 4 hours, reappears in the organism of uninjected nurslings after passing through the organism of the mother. The amount of 131I transferred from injected rats into the bodies of isolated uninjected rats of the same litter decreased during the period of weaning. The observed recirculation of 131I between immature rats and their mothers in both directions may represent a saving mechanism which might include several other substances and would compensate for their loss via the milk, and suggests a new aspect of maternal–neonatal interrelationship which appears as a continuation of the state existing in utero.

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