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.

Mechanisms and regulation of water permeability in renal epithelia

1989 ◽  
Vol 257 (5) ◽  
pp. C837-C850 ◽  
Author(s):  
A. S. Verkman
Keyword(s):  
Urinary Bladder ◽  
Proximal Tubule ◽  
Water Permeability ◽  
Permeability Coefficient ◽  
Biological Membranes ◽  
Water Channels ◽  
Proton Pumps ◽  
Toad Urinary Bladder ◽  
Water Permeability Coefficient ◽  
Collecting Tubule

Water transport occurs in all biological membranes. A few selected membranes in the kidney, amphibian urinary bladder, and erythrocyte have very high water permeability and are thought to contain specialized water transporting units termed "water channels." The known biophysical properties of membranes containing water channels are a high osmotic water permeability coefficient (Pf), an osmotic-to-diffusional water permeability coefficient ratio (Pf/Pd) greater than unity, a low activation energy (Ea), and inhibition by mercurial compounds. The biochemical and molecular characteristics of water channel pathways are not known at present. Established and new methods to measure Pf and Pd in kidney tubules and in isolated membrane vesicles from kidney cells are reviewed and evaluated. In the mammalian proximal tubule, a high Pf results from transcellular movement of water across highly permeable apical and basolateral membranes containing water channels. It has been assumed that proximal tubule Pf is unregulated; however, recent results indicate that apical water channels are retrieved by endocytosis and that Pf is decreased fivefold with increasing transepithelial osmotic gradients. In the thin and thick ascending limbs, Pf is nearly the lowest of all biological membranes and is not subject to regulation. In contrast, collecting tubule Pf is subject to hormonal regulation by vasopressin. Vasopressin binding to receptors located at the basal membrane of principal cells initiates adenosine 3',5'-cyclic monophosphate production, which is thought ultimately to activate the exocytic insertion of intracellular vesicles containing water channels into the cell apical membrane. Vasopressin-induced endosomes from kidney collecting tubule and toad urinary bladder contain functional water channels but no proton pumps or urea transporters, supporting a membrane shuttle hypothesis that is selective for water channels. Future directions for the isolation and molecular cloning of kidney water channels are evaluated.

scholarly journals Nature of the water permeability increase induced by antidiuretic hormone (ADH) in toad urinary bladder and related tissues.

1976 ◽  
Vol 68 (2) ◽  
pp. 137-143 ◽  
Author(s):  
A Finkelstein
Keyword(s):  
Urinary Bladder ◽  
Cell Membrane ◽  
Antidiuretic Hormone ◽  
Lipid Bilayers ◽  
Water Permeability ◽  
Permeability Coefficient ◽  
Diffusion Mechanism ◽  
Toad Urinary Bladder ◽  
Lipid Bilayer Membranes ◽  
Water Permeability Coefficient

In artificial lipid bilayer membranes, the ratio of the water permeability coefficient (Pd(water)) to the permeability coefficient of an arbitrary nonelectrolyte such as n-butyramide (Pd(n-butyramide)) remains relatively constant with changes in lipid composition and temperature, even though the individual Pd's increase more than 100-fold. I propose that this is a general rule that also holds for the lipid bilayers of cells and tissues, and that therefore if Pd(water)/Pd(solute greatly exceeds the value found for artifical lipid bilayers (where "solute" is a molecule, such as 1,6 hexanediol or n-butyramide, that crosses the cell membrane by a solubility-diffusion mechanism without the aid of a special transporting system), then water crosses the cell membrane via aqueous pores. Applying this criterion to the toad urinary bladder, we find that even in the unstimulated bladder, water probably crosses the luminal membrane primarily through small aqueous pores, and that this almost certainly the case after antidiuretic hormone (ADH) stimulation. I suggest that ADH stimulation ultimately leads either to formation (or enlargement) of pores, by the rearrangement of preexisting subunits, or to an unplugging of these pores.

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.

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.

scholarly journals Osmosis in Cortical Collecting Tubules

1974 ◽  
Vol 64 (2) ◽  
pp. 201-228 ◽  
Author(s):  
James A. Schafer ◽  
Clifford S. Patlak ◽  
Thomas E. Andreoli
Keyword(s):  
Steady State ◽  
Water Permeability ◽  
Permeability Coefficient ◽  
Osmotic Water Permeability ◽  
Osmotic Flow ◽  
Unstirred Layers ◽  
Water Permeability Coefficient ◽  
Osmotic Water ◽  
In Series ◽  
Collecting Tubules

This paper reports a theoretical analysis of osmotic transients and an experimental evaluation both of rapid time resolution of lumen to bath osmosis and of bidirectional steady-state osmosis in isolated rabbit cortical collecting tubules exposed to antidiuretic hormone (ADH). For the case of a membrane in series with unstirred layers, there may be considerable differences between initial and steady-state osmotic flows (i.e., the osmotic transient phenomenon), because the solute concentrations at the interfaces between membrane and unstirred layers may vary with time. A numerical solution of the equation of continuity provided a means for computing these time-dependent values, and, accordingly, the variation of osmotic flow with time for a given set of parameters including: Pf (cm s–1), the osmotic water permeability coefficient, the bulk phase solute concentrations, the unstirred layer thickness on either side of the membrane, and the fractional areas available for volume flow in the unstirred layers. The analyses provide a quantitative frame of reference for evaluating osmotic transients observed in epithelia in series with asymmetrical unstirred layers and indicate that, for such epithelia, Pf determinations from steady-state osmotic flows may result in gross underestimates of osmotic water permeability. In earlier studies, we suggested that the discrepancy between the ADH-dependent values of Pf and PDDw (cm s–1, diffusional water permeability coefficient) was the consequence of cellular constraints to diffusion. In the present experiments, no transients were detectable 20–30 s after initiating ADH-dependent lumen to bath osmosis; and steady-state ADH-dependent osmotic flows from bath to lumen and lumen to bath were linear and symmetrical. An evaluation of these data in terms of the analytical model indicates: First, cellular constraints to diffusion in cortical collecting tubules could be rationalized in terms of a 25-fold reduction in the area of the cell layer available for water transport, possibly due in part to transcellular shunting of osmotic flow; and second, such cellular constraints resulted in relatively small, approximately 15%, underestimates of Pf.

Actin filaments and vasopressin-stimulated water flow in toad urinary bladder

1983 ◽  
Vol 245 (1) ◽  
pp. C28-C39 ◽  
Author(s):  
M. Pearl ◽  
A. Taylor
Keyword(s):  
Epithelial Cells ◽  
Urinary Bladder ◽  
Water Permeability ◽  
Plasma Membranes ◽  
Cytochalasin B ◽  
Specific Inhibitor ◽  
Indirect Evidence ◽  
Toad Urinary Bladder ◽  
Cytoplasmic Organelle ◽  
Morphological Studies

Vasopressin increases the water permeability of the apical membrane of the granular epithelial cells of the toad urinary bladder. Cytochalasin B inhibits this action of the hormone, indicating that microfilaments may play a role in the water permeability response. We have extended previous functional studies with cytochalasin B and have demonstrated that dihydrocytochalasin B, a more specific inhibitor of actin filament elongation, similarly diminishes the hydrosmotic response to vasopressin. Biochemical studies of isolated epithelial cells indicate that an actin-like protein accounts for about 10% of the soluble protein of the epithelium. Morphological studies of whole toad bladders incubated with heavy meromyosin conclusively demonstrate that actin is a component of the epithelial cells and that actin-containing filaments are associated with both plasma membranes and cytoplasmic organelle membranes. Taken together, these findings provide strong, albeit indirect, evidence that actin microfilaments play a functional role in the hormone-induced increase in water permeability in the toad urinary bladder.

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.

scholarly journals Water Permeability of Thin Lipid Membranes

1967 ◽  
Vol 50 (6) ◽  
pp. 1765-1784 ◽  
Author(s):  
Albert Cass ◽  
Alan Finkelstein
Keyword(s):  
Water Permeability ◽  
Electrical Resistance ◽  
Lipid Membranes ◽  
Permeability Coefficient ◽  
Plasma Membranes ◽  
Brain Lipids ◽  
Osmotic Permeability ◽  
Unstirred Layers ◽  
Water Permeability Coefficient

The osmotic permeability coefficient, Pf, and the tagged water permeability coefficient, Pd, were determined for thin (<100 A) lipid membranes formed from ox brain lipids plus DL-α-tocopherol; their value of approximately 1 x 10-3 cm/sec is within the range reported for plasma membranes. It was established that Pf = Pd. Other reports that Pf > Pd can be attributed to the presence of unstirred layers in the experimental determination of Pd. Thus, there is no evidence for the existence of aqueous pores in these thin phospholipid membranes. The adsorption onto the membrane of a protein that lowers its electrical resistance by a factor of 103 was found not to affect its water permeability; however, glucose and sucrose were found to interact with the membrane to modify Pf. Possible mechanisms of water transport across these films are discussed, together with the implications of data obtained on these structures for plasma membranes.

scholarly journals Impact of Biochar on Soil Water Permeability Coefficient During 2 Year Field Experiment

2020 ◽  
Vol 609 ◽  
pp. 012108
Author(s):  
Maciej Gliniak ◽  
Jakub Sikora ◽  
Urszula Sadowska ◽  
Agnieszka Klimek-Kopyra ◽  
Agnieszka Latawiec ◽  
...  
Keyword(s):  
Field Experiment ◽  
Soil Water ◽  
Water Permeability ◽  
Permeability Coefficient ◽  
Water Permeability Coefficient
Sign in / Sign up

Export Citation Format

Share Document