scholarly journals Very high water permeability in vasopressin-induced endocytic vesicles from toad urinary bladder.

1989 ◽  
Vol 94 (6) ◽  
pp. 1101-1115 ◽  
Author(s):  
L B Shi ◽  
A S Verkman
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Time Course ◽  
Toad Urinary Bladder ◽  
Stopped Flow ◽  
Osmotic Water Permeability ◽  
Luminal Membrane ◽  
Osmotic Water ◽  
Group A ◽  
Endocytic Vesicles

The regulation of transepithelial water permeability in toad urinary bladder is believed to involve a cycling of endocytic vesicles containing water transporters between an intracellular compartment and the cell luminal membrane. Endocytic vesicles arising from luminal membrane were labeled selectively in the intact toad bladder with the impermeant fluid-phase markers 6-carboxyfluorescein (6CF) or fluorescein-dextran. A microsomal preparation containing labeled endocytic vesicles was prepared by cell scraping, homogenization, and differential centrifugation. Osmotic water permeability was measured by a stopped-flow fluorescence technique in which microsomes containing 50 mM mannitol, 5 mM K phosphate, pH 8.5 were subject to a 60-mM inwardly directed gradient of sucrose; the time course of endosome volume, representing osmotic water transport, was inferred from the time course of fluorescence self-quenching. Endocytic vesicles were prepared from toad bladders with hypoosmotic lumen solution treated with (group A) or without (group B) serosal vasopressin at 23 degrees C, and bladders in which endocytosis was inhibited by treatment with vasopressin at 0-2 degrees C (group C), or with vasopressin plus sodium azide at 23 degrees C (group D). Stopped-flow results in all four groups showed a slow rate of 6CF fluorescence decrease (time constants 1.0-1.7 s for exponential fit) indicating a component of nonendocytic 6CF entrapment into sealed vesicles. However, in vesicles from group A only, there was a very rapid 6CF fluorescence decrease (time constant 9.6 +/- 0.2 ms, SEM, 18 separate preparations) with an osmotic water permeability coefficient (Pf) of greater than 0.1 cm/s (18 degrees C) and activation energy of 3.9 +/- 0.8 kcal/mol (16 kJ/mol). Pf was inhibited reversibly by greater than 60% by 1 mM HgCl2. The rapid fluorescence decrease was absent in vesicles in groups B, C, and D. These results demonstrate the presence of functional water transporters in vasopressin-induced endocytic vesicles from toad bladder, supporting the hypothesis that water channels are cycled to and from the luminal membrane and providing a functional marker for the vasopressin-sensitive water channel. The calculated Pf in the vasopressin-induced endocytic vesicles is the highest Pf reported for any biological or artificial membrane.

Relation of ADH effects to altered membrane fluidity in toad urinary bladder

1981 ◽  
Vol 240 (1) ◽  
pp. F63-F69
Author(s):  
W. A. Kachadorian ◽  
J. Muller ◽  
S. Rudich ◽  
V. A. DiScala
Keyword(s):  
Urinary Bladder ◽  
Membrane Fluidity ◽  
Water Permeability ◽  
Membrane Lipids ◽  
Granular Cell ◽  
Toad Urinary Bladder ◽  
Osmotic Water Permeability ◽  
Intramembranous Particle ◽  
Luminal Membrane ◽  
Osmotic Water

Membrane fluidity, urea permeability, and osmotic water permeability in toad urinary bladder are regularly enhanced by antidiuretic hormone (ADH). In addition, organized intramembranous particle aggregates, which correlate specifically with hormonally stimulated water permeability, are found in granular cell luminal membranes consequent to ADH stimulation. In this investigation ADH-stimulated changes in urea and osmotic water permeability and luminal membrane aggregates at room temperature (24.8 +/- 0.4 degrees C) and in the cold 10.6 +/- 0.2 degrees) were compared with corresponding changes in membrane fluidity, as assessed by n-butyramide permeability. Although a critical level of membrane fluidity is undoubtedly required, the occurrence of aggregates in the luminal membrane is independent of an accompanying hormonally induced change of membrane fluidity. ADH-stimulated osmotic water permeability in toad bladder is also independent of the coincident change in membrane fluidity, and as a process almost certainly involves membrane channels, not a solubility-diffusion process through membrane lipids. For ADH-stimulated transbladder urea movement, channels seem to be involved as well, and the change induced in membrane fluidity by ADH could be an underlying factor in their formation.

AVP-independent high osmotic water permeability of frog urinary bladder and autacoids

1996 ◽  
Vol 433 (1-2) ◽  
pp. 136-145 ◽  
Author(s):  
Y. V. Natochin ◽  
R. G. Parnova ◽  
E. I. Shakhmatova ◽  
Y. Y. Komissarchik ◽  
M. S. Brudnaya ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Osmotic Water Permeability ◽  
Frog Urinary Bladder ◽  
Osmotic Water

Effects of serosal hypertonicity on water permeability in toad urinary bladder

1990 ◽  
Vol 258 (5) ◽  
pp. C871-C878 ◽  
Author(s):  
W. A. Kachadorian ◽  
K. R. Spring ◽  
N. L. Shinowara ◽  
J. Muller ◽  
T. A. Palaia ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Water Movement ◽  
Granular Cell ◽  
Toad Urinary Bladder ◽  
Morphological Examination ◽  
Tissue Water ◽  
Coated Pits ◽  
Thin Sections ◽  
Luminal Membrane

We studied in toad urinary bladder the effects of serosal hypertonicity on tissue water permeability, granular cell luminal membrane water permeability, and granular cell luminal membrane particle aggregates and compared them with effects of antidiuretic hormone (ADH). In tissues challenged by a hypertonic (447 mosmol/kgH2O) serosal bath, luminal membrane aggregates were structurally similar to those caused by ADH. The tissue water permeability increase induced by serosal hypertonicity was much less than that caused by a maximally stimulating concentration of ADH on tissue in isotonic serosal baths with approximately the same transmural gradient. The difference is explained not only by a reduced incidence of luminal membrane aggregates but also by an increased resistance to water movement at a postluminal membrane site. Measurements of luminal membrane water permeability showed a close correlation with luminal membrane aggregate frequency, indicating that the calculated permeability of an individual aggregate was a constant. Thus the relation of luminal membrane aggregates to tissue osmotic permeability is modified by serosal hypertonicity. Morphological examination of these tissues suggested that luminal membrane aggregates may be less stable in the absence of hormone. This was evident by the proportionally greater number of structures interpreted as aggregates captured in the process of disassembly ("patches"). Membrane depressions containing intramembrane particles ("craters") were also observed. They corresponded in terms of frequency and size to coated pits as seen in thin sections.

A Stopped-Flow Light Scattering Methodology for Assessing the Osmotic Water Permeability of Whole Sertoli Cells

2018 ◽  
pp. 279-286 ◽  
Author(s):  
Anna Maggio ◽  
Raquel L. Bernardino ◽  
Patrizia Gena ◽  
Marco G. Alves ◽  
Pedro F. Oliveira ◽  
...  
Keyword(s):  
Light Scattering ◽  
Water Permeability ◽  
Sertoli Cells ◽  
Stopped Flow ◽  
Osmotic Water Permeability ◽  
Osmotic Water

Prostaglandin-dependent osmotic water permeability of the frog and trout urinary bladder

1998 ◽  
Vol 121 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Yu.V. Natochin ◽  
E.I. Shakhmatova ◽  
Ya.Yu. Komissarchik ◽  
E.S. Snigirevskaya ◽  
N.P. Prutskova ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Osmotic Water Permeability ◽  
Osmotic Water

Prostaglandin E2 inhibits vasotocin-induced osmotic water permeability in the frog urinary bladder by EP1-receptor-mediated activation of NO/cGMP pathway

2007 ◽  
Vol 293 (1) ◽  
pp. R528-R537 ◽  
Author(s):  
Vera Bachteeva ◽  
Ekaterina Fock ◽  
Elena Lavrova ◽  
Svetlana Nikolaeva ◽  
Stepan Gambaryan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Urinary Bladder ◽  
Water Permeability ◽  
Inhibitory Effect ◽  
No Synthase ◽  
Arginine Vasotocin ◽  
Osmotic Water Permeability ◽  
Frog Urinary Bladder ◽  
Osmotic Water ◽  
Cgmp Pathway

PGE2 is a well-known inhibitor of the antidiuretic hormone-induced increase of osmotic water permeability (OWP) in different osmoregulatory epithelia; however, the mechanisms underlying this effect of PGE2 are not completely understood. Here, we report that, in the frog Rana temporaria urinary bladder, EP1-receptor-mediated inhibition of arginine-vasotocin (AVT)-induced OWP by PGE2 is attributed to increased generation of nitric oxide (NO) in epithelial cells. It was shown that the inhibitory effect of 17-phenyl-trinor-PGE2 (17-ph-PGE2), an EP1 agonist, on AVT-induced OWP was significantly reduced in the presence of 7-nitroindazole (7-NI), a neuronal NO synthase (nNOS) inhibitor. NO synthase (NOS) activity in both lysed and intact epithelial cells measured as a rate of conversion of l-[3H]arginine to l-[3H]citrulline was Ca2+ dependent and inhibited by 7-NI. PGE2 and 17-ph-PGE2, but not M&B-28767 (EP3 agonist) or butaprost (EP2 agonist), stimulated NOS activity in epithelial cells. The above effect of PGE2 was abolished in the presence of SC-19220, an EP1 antagonist. 7-NI reduced the stimulatory effect of 17-ph-PGE2 on NOS activity. 17-ph-PGE2 increased intracellular Ca2+ concentration and cGMP in epithelial cells. Western blot analysis revealed an nNOS expression in epithelial cells. These results show that the inhibitory effect of PGE2 on AVT-induced OWP in the frog urinary bladder is based at least partly on EP1-receptor-mediated activation of the NO/cGMP pathway, suggesting a novel cross talk between AVT, PGE2, and nNOS that may be important in the regulation of water transport.

Epithelial organization and hormone sensitivity of toad urinary bladder cells in culture

1981 ◽  
Vol 241 (2) ◽  
pp. F129-F138 ◽  
Author(s):  
J. P. Johnson ◽  
R. E. Steele ◽  
F. M. Perkins ◽  
J. B. Wade ◽  
A. S. Preston ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Cell Line ◽  
Cell Lines ◽  
Water Permeability ◽  
Sodium Transport ◽  
Time Course ◽  
Cultured Cells ◽  
Transepithelial Transport ◽  
Seeding Density ◽  
Toad Urinary Bladder

Two continuous cell lines (TB-M and TB-6c) derived from epithelial cells of the toad urinary bladder form epithelia in culture that manifest hormone-sensitive transepithelial transport. Development of transepithelial electrical resistance (R) and transport rate (ISC) are dependent on time and density of cells seeded, but steady-state ISC and R are characteristic for each cell line and independent of seeding density. Some responses of intact toad bladder are preserved in culture, whereas others are altered or absent. Neither cell line responds to vasopressin. Analogues of cAMP increase sodium transport and urea permeability in both cell lines but do not affect water permeability. The intramembrane particle aggregates associated with the vasopressin- and cAMP-induced increase in water permeability of the intact bladder could not be detected in the cell lines. Aldosterone increases sodium transport in both cell lines, and the time course and concentration dependence of the response to aldosterone are similar to those of the intact bladder. The relative effect of a series of steroids on ISC reveals corticosterone to be a more potent mineralocorticoid in cultured cells than in the intact bladder.

scholarly journals The water permeability of toad urinary bladder. I. Permeability of barriers in series with the luminal membrane.

1984 ◽  
Vol 83 (4) ◽  
pp. 529-541 ◽  
Author(s):  
S D Levine ◽  
M Jacoby ◽  
A Finkelstein
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Permeability Coefficient ◽  
Plasma Membranes ◽  
Toad Urinary Bladder ◽  
Luminal Membrane ◽  
Water Permeability Coefficient ◽  
In Series ◽  
Aqueous Layer ◽  
Lipophilic Component

Antidiuretic hormone (ADH) induces a large increase in the water permeability of the luminal membrane of toad urinary bladder. Measured values of the diffusional water permeability coefficient, Pd(w), are spuriously low, however, because of barriers within the tissue, in series with the luminal membrane, that impede diffusion. We have now determined the water permeability coefficient of these series barriers in fully stretched bladders and find it to be approximately 6.3 X 10(-4) cm/s. This is equivalent to an unstirred aqueous layer of approximately 400 microns. On the other hand, the permeability coefficient of the bladder to a lipophilic molecule, hexanol, is approximately 9.0 X 10(-4) cm/s. This is equivalent to an unstirred aqueous layer of only 100 microns. The much smaller hindrance to hexanol diffusion than to water diffusion by the series barriers implies a lipophilic component to the barriers. We suggest that membrane-enclosed organelles may be so tightly packed within the cytoplasm of granular epithelial cells that they offer a substantial impediment to diffusion of water through the cell. Alternatively, the lipophilic component of the barrier could be the plasma membranes of the basal cells, which cover most of the basement membrane and thereby may restrict water transport to the narrow spaces between basal and granular cells.

ADH or theophylline-induced changes in intracellular free and membrane-bound calcium

1984 ◽  
Vol 247 (6) ◽  
pp. F939-F945 ◽  
Author(s):  
R. M. Burch ◽  
P. V. Halushka
Keyword(s):  
Plasma Membrane ◽  
Epithelial Cells ◽  
Urinary Bladder ◽  
Antidiuretic Hormone ◽  
Water Permeability ◽  
Time Course ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Membrane Bound ◽  
Induced Changes

Ca2+ is thought to play a role in the enhancement of water permeability of toad urinary bladder epithelial cells by antidiuretic hormone (ADH) or theophylline. This study examined the effects of ADH and theophylline on intracellular free Ca2+ ([Ca2+]i) and total cellular exchangeable Ca2+ in isolated toad bladder epithelial cells. ADH or theophylline enhanced water permeability maximally by 15-25 min after a 4-min lag. 45Ca2+ efflux, a probe for total cellular exchangeable (plasma membrane plus intracellular) Ca2+, was enhanced by ADH within 2 min and returned to control by 8 min. Chlortetracycline fluorescence, a probe for intracellular Ca2+ only, was not affected, suggesting that ADH released only plasma membrane-bound Ca2+. Theophylline enhanced 45Ca2+ efflux and decreased chlortetracycline fluorescence, suggesting release of Ca2+ from intracellular sources. Both agents decreased [Ca2+]i as assessed by quin-2 fluorescence with a time course similar to the enhancement in water permeability. The results suggest that the changes in membrane-bound Ca2+ and [Ca2+]i induced by ADH and theophylline may play a role in the enhanced permeability to water in response to these agents.

Unimpaired osmotic water permeability and fluid secretion in bile duct epithelia of AQP1 null mice

2002 ◽  
Vol 283 (3) ◽  
pp. G739-G746 ◽  
Author(s):  
Albert Mennone ◽  
Alan S. Verkman ◽  
James L. Boyer
Keyword(s):  
Bile Duct ◽  
Cyclic Amp ◽  
Water Permeability ◽  
Water Movement ◽  
Fluid Secretion ◽  
Osmotic Gradient ◽  
Osmotic Water Permeability ◽  
Luminal Membrane ◽  
Osmotic Water ◽  
Aqp1 Expression

The mechanisms by which fluid moves across the luminal membrane of cholangiocyte epithelia are uncertain. Previous studies suggested that aquaporin-1 (AQP1) is an important determinant of water movement in rat cholangiocytes and that cyclic AMP mediates the movement of these water channels from cytoplasm to apical membrane, thereby increasing the osmotic water permeability. To test this possibility we measured agonist-stimulated fluid secretion and osmotically driven water transport in isolated bile duct units (IBDUs) from AQP1 wild-type (+/+) and null (−/−) mice. AQP1 expression was confirmed in a mouse cholangiocyte cell line and +/+ liver. Forskolin-induced fluid secretion, measured from the kinetics of IBDU luminal expansion, was 0.05 fl/min and was not impaired in −/− mice. Osmotic water permeability (Pf), measured from the initial rate of IBDU swelling in response to a 70-mosM osmotic gradient, was 11.1 × 10−4 cm/s in +/+ mice and 11.5 × 10−4cm/s in −/− mice. Pf values increased by ∼50% in both +/+ and −/− mice following preincubation with forskolin. These findings provide direct evidence that AQP1 is not rate limiting for water movement in mouse cholangiocytes and does not appear to be regulated by cyclic AMP in this species.

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