Isolation and characterization of specialized regions of toad urinary bladder apical plasma membrane involved in the water permeability response to antidiuretic hormone

1987 ◽  
Vol 96 (2) ◽  
pp. 175-186 ◽  
Author(s):  
H. William Harris ◽  
Helen R. Murphy ◽  
Mark C. Willingham ◽  
Joseph S. Handler
Keyword(s):  
Plasma Membrane ◽  
Urinary Bladder ◽  
Antidiuretic Hormone ◽  
Water Permeability ◽  
Apical Plasma Membrane ◽  
Toad Urinary Bladder ◽  
Isolation And Characterization

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.

Modulation of antidiuretic hormone-dependent capacitance and water flow in toad urinary bladder

1984 ◽  
Vol 246 (4) ◽  
pp. F501-F508
Author(s):  
L. G. Palmer ◽  
N. Speez
Keyword(s):  
Urinary Bladder ◽  
Antidiuretic Hormone ◽  
Water Flow ◽  
Water Permeability ◽  
Apical Membrane ◽  
Toad Urinary Bladder ◽  
Osmotic Gradient ◽  
Apical Surface ◽  
Membrane Area ◽  
Close Relationship

To test the hypothesis that antidiuretic hormone- (ADH) dependent water permeability is associated with changes in apical membrane area, hormone-dependent water flow and capacitance changes were measured in the toad urinary bladder under a number of different conditions. Dose-response relationships for water flow (Jv) and capacitance increases (delta C) were similar from 1 to 20 mU/ml ADH. At higher concentrations, Jv reached a plateau, while delta C decreased. The decrease in delta C was prevented by elimination of the osmotic gradient across the tissue. Serosal hydrazine (10 mM) increased Jv sevenfold and delta C threefold in the presence of 1 mU/ml ADH. Mucosal NH4Cl, at constant mucosal pH, increased Jv by 50-100%, but did not significantly change delta C. In the absence of an osmotic gradient, mucosal NH+4 increased delta C by 50%. NH4Cl had no effect on hydroosmotic response to 8-bromo-adenosine 3',5'-cyclic monophosphate (cAMP). Mucosal CO2 (9%) decreased Jv by greater than 90%, and delta C by 60% with 20 mU/ml ADH. Mucosal CO2 also inhibited the hydroosmotic response to 8-bromo-cAMP. Removal of serosal Na diminished cAMP-dependent Jv and delta C. The results confirmed the close relationship between ADH-dependent water permeability and membrane capacitance. They indicate, however, that under some circumstances membrane may be retrieved from the apical surface without affecting water permeability.

Antidiuretic hormone moves membranes

1988 ◽  
Vol 255 (3) ◽  
pp. F375-F382 ◽  
Author(s):  
J. S. Handler
Keyword(s):  
Plasma Membrane ◽  
Antidiuretic Hormone ◽  
Water Permeability ◽  
Apical Membrane ◽  
Collecting Duct ◽  
Toad Bladder ◽  
Cell Swelling ◽  
Apical Plasma Membrane ◽  
Principal Cells ◽  
Particle Aggregates

This review focuses on events at the apical plasma membrane of toad urinary bladder and mammalian collecting duct as their permeability to water changes in response to antidiuretic hormone (ADH) and to its withdrawal. The major marker of the permeability change is observed in freeze-fracture electron microscopy of the apical plasma membrane and consists of a dramatic increase in membrane particle aggregates and, in toad bladder but not in collecting duct, in fused vesicles (aggrephores) that contain particle aggregates in their limiting membranes. Withdrawal of ADH is accompanied by endocytosis at the apical membrane, reflecting retrieval of water-permeable, particle aggregate-containing membrane. Covalent labeling of the external surface of the apical membrane of toad bladder identifies specific proteins that are present in the apical membrane only during the response to ADH. Proteins of the same molecular weights are also present in the retrieved membrane when ADH is withdrawn. Several controversial areas are considered, including the extent of cell swelling as water flows across the epithelium from dilute apical solution to isotonic basal solution, whether only principal cells or principal cells and intercalated cells participate in the water permeability response of the collecting duct, the role of the cytoskeleton in the water permeability response, and the proposed second water permeability barrier that is affected by ADH, but not by adenosine 3',5'-cyclic monophosphate.

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.

scholarly journals Antidiuretic hormone modulates membrane phosphoproteins in toad urinary bladder and retrieved water channel containing apical membrane vesicles.

1991 ◽  
Vol 1 (9) ◽  
pp. 1114-1122
Author(s):  
H W Harris
Keyword(s):  
Membrane Proteins ◽  
Urinary Bladder ◽  
Membrane Protein ◽  
Antidiuretic Hormone ◽  
Water Permeability ◽  
Apical Membrane ◽  
Water Channel ◽  
Water Channels ◽  
Toad Urinary Bladder ◽  
Granular Cells

Antidiuretic hormone (ADH) dramatically increases the water permeability of toad urinary bladder by insertion of unique highly selective water channels into the apical membranes of granular cells. Before ADH stimulation, water channels are stored in high concentrations in the limiting membranes of large cytoplasmic vesicles called aggrephores. ADH stimulation causes aggrephore fusion with the granular cell apical membrane and increases water permeability. Transepithelial osmotic water flow causes a rapid attenuation of the ADH-elicited increase in water permeability through a process called flux inhibition. Flux inhibition is due to retrieval of ADH water channels by apical membrane endocytosis. When phosphoproteins of intact bladders are labeled with (32P)orthophosphate, the 32P content of 34-, 28-, and 17-kDa proteins is increased by ADH stimulation. When flux inhibition occurs, the 32P-labelling of a 15.5-kDa protein is reduced to approximately one half its original value (Konieczkowski M, Rudolph SA, J Pharmacol Exp Ther 1985;234:515). These observations have been confirmed, and these studies have been extended, by using a combination of subcellular fractionation and membrane protein chemistry techniques. All four of these phosphoproteins are present in membrane fractions of granular cells. Analysis of membrane proteins by a combination of Triton X-114 partitioning and an alkaline stripping technique reveals that the 28- and 17-kDa species are integral membrane proteins of unknown function. In contrast, the 32P-labeled 15.5-kDa protein is a peripheral membrane protein. It is attached to the cytoplasmic (outer) surface of highly water-permeable vesicles retrieved during flux inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

ADH-induced recycling of fluid-phase marker from endosomes to the mucosal surface in toad bladder

1994 ◽  
Vol 267 (1) ◽  
pp. C32-C38 ◽  
Author(s):  
R. A. Coleman ◽  
J. B. Wade
Keyword(s):  
Urinary Bladder ◽  
Horseradish Peroxidase ◽  
Antidiuretic Hormone ◽  
Water Permeability ◽  
Apical Membrane ◽  
Fluid Phase ◽  
Water Channels ◽  
Toad Urinary Bladder ◽  
Bathing Solution ◽  
Apical Surface

In the toad urinary bladder, the reversal of antidiuretic hormone (ADH) stimulation results in the endocytosis of apical membrane water channels, along with any fluid-phase marker present in the mucosal bathing solution. We have loaded vesicles with horseradish peroxidase (HRP), then restimulated the bladders and measured the reappearance of endocytosed HRP in the mucosal bath. HRP-loaded bladders that were restimulated showed HRP release that peaked sharply within 15 min after restimulation. Varying the interval between loading and restimulation did not vary HRP release significantly. Restimulation with forskolin gave HRP release values similar to ADH. The amount of HRP released correlated with the magnitude of water permeability induced. The demonstration that fluid-phase markers can be recycled from endosomes to the apical surface in a hormone-dependent fashion indicates that endocytosed membrane, containing water channels, is able to rapidly recycle back to the surface in response to hormone restimulation. In addition, marker release declined progressively with repeated restimulation, totaling < 30% of the retrieved amount. This result indicates that a relatively large proportion of the retrieved marker reaches a nonrecycling compartment.

scholarly journals Role of osmotic forces in exocytosis: studies of ADH-induced fusion in toad urinary bladder.

1981 ◽  
Vol 91 (2) ◽  
pp. 584-588 ◽  
Author(s):  
W A Kachadorian ◽  
J Muller ◽  
A Finkelstein
Keyword(s):  
Plasma Membrane ◽  
Urinary Bladder ◽  
Antidiuretic Hormone ◽  
Basic Mechanism ◽  
Toad Urinary Bladder ◽  
Bathing Medium ◽  
Intramembrane Particle ◽  
Luminal Membrane ◽  
Particle Aggregates

Antidiuretic hormone (ADH) treatment of toad urinary bladder activates an exocytotic-like process by which intramembrane particle aggregates are transferred from membranes of elongated cytoplasmic tubules to the luminal-facing plasma membrane. We find that the number of these ADH-induced fusion events, and the number of aggregates appearing in the luminal membrane, are reduced when the luminal bathing medium is made hyperosmotic. As an apparent consequence of the inhibition of their fusion with the luminal membrane, the elongated cytoplasmic tubules become enormously swollen into large, rounded vesicles. These results are consistent with the view that osmotic forces are essential to the basic mechanism of exocytosis.

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