Polycations reduce vasopressin-induced water flow by endocytic removal of water channels

1986 ◽  
Vol 250 (5) ◽  
pp. C729-C737 ◽  
Author(s):  
R. Beauwens ◽  
G. te Kronnie ◽  
J. Snauwaert ◽  
P. A. in't Veld
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Sodium Channels ◽  
Sodium Transport ◽  
Water Channels ◽  
Toad Urinary Bladder ◽  
Cationized Ferritin ◽  
Ultrastructural Studies ◽  
Urea Permeability ◽  
Luminal Cells

Several polycations added to the luminal solution were found to inhibit the vasopressin (ADH)-induced water flow in toad urinary bladder but not the ADH-induced increase in sodium transport or in urea permeability. Ultrastructural studies were conducted to evaluate the uptake of cationized ferritin. It was found that endocytosis of cationized ferritin by luminal cells was strikingly enhanced on exposure to ADH; this increased endocytosis was concomitant with inhibition of transepithelial ADH-induced water flow. Various maneuvers preventing endocytosis were also found to counteract the polycation-induced inhibition of the ADH effect. It is suggested that polycations are endocytosed in vesicles whose walls contain the water channels but not the urea or sodium channels.

Alterations in surface substructure and degranulation of subapical cytoplasmic granules by mezereinu (MZ) in toad urinary bladder epithelia

1989 ◽  
Vol 47 ◽  
pp. 916-917
Author(s):  
A. J. Mia ◽  
L. X. Oakfoid ◽  
T. Yorio
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Urinary Bladder ◽  
Water Flow ◽  
Apical Membrane ◽  
Water Channels ◽  
Phosphoinositide Metabolism ◽  
Apical Surface ◽  
Ultrastructural Studies ◽  
Kinase C

The increase in transepithelial water flow induced by antidiuretic hormone (ADH) occurs through the ADH V2 receptor, and includes the stimulation of adenylcyclase, an increase in cAMP synthesis and the activation of protein kinase A. These biochemical events in amphibian urinary bladder tissues are reported to be accompanied by apical membrane transformations including the induction of numerous microvilli, and an increase in apical surface area as a result of incorporation of water channels. Amphibian epithelia also contain an ADH V1 receptor coupled to phosphoinositide metabolism and inositol phosphate release. Recently, it was demonstrated that mezerein (MZ), a non-phorbol activator of protein kinase C (PKC)increased transepithelial water flow when added to mucosal surface. The magnitude of water transport was less and occurred over a longer period of time than compared to ADH-stimulated tissues (7,and also Table 1). However, there is little or no information available on ultrastructural studies linking the events due to the ADH V1 receptor and osmotic water flow. Presently, we report on morphological and cytological observations which suggests that the ADH V1 receptor cascade may play a role in the insertion of water channels into the apical membrane possibly through the activation of PKC. The present study utilizes mezerein (MZ), a non-phorbol activator of protein kinase C (PKC) to examine the effect of MZ on epithelial cytomorphology.

Cytosolic calcium and the action of vasopressin in toad urinary bladder

1987 ◽  
Vol 252 (6) ◽  
pp. F1028-F1041
Author(s):  
A. Taylor ◽  
E. Eich ◽  
M. Pearl ◽  
A. S. Brem ◽  
E. Q. Peeper
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Sodium Transport ◽  
Short Circuit ◽  
Exchange Process ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Toad Urinary Bladder ◽  
Low Sodium ◽  
Transepithelial Sodium Transport

The effects of experimental procedures believed to increase cytosolic calcium on basal and vasopressin-stimulated osmotic water flow and transepithelial sodium transport were examined in the toad urinary bladder. Exposure of isolated toad bladders to quinidine, calcium ionophores (A23187, X537A), or low-sodium or potassium-free serosal solutions resulted in a dose-dependent decrease in the hydrosmotic response to vasopressin or exogenous adenosine 3',5'-cyclic monophosphate (cAMP). The degree of inhibition of cAMP-induced water flow induced by low-sodium or potassium-free serosal bathing media varied, and in a similar manner, with the serosal calcium concentration. The effects of quinidine sulfate (2 X 10-4 M), X537A (2 X 10(-5) M), and low serosal sodium (20 mM), but not that of A23187 (10(-5) M), were readily reversible. Exposure to quinidine (4 X 10(-4) M), A23187 (10(-5) M), X537A (5 X 10(-6) M), or low serosal sodium (2 mM) also inhibited the basal short-circuit current (SCC). Vasopressin, 4-20 mU/ml, completely overcame the inhibition of the SCC induced by quinidine, A23187, or low serosal sodium, but a submaximal dose of hormone (4 mU/ml) failed to fully reverse the inhibitory effect of X537A, 5 X 10(-6) M. These results are consistent with the view that 1) a Na-Ca exchange process operates across the basolateral surface of the granular epithelial cells of the toad urinary bladder in vivo, and 2) the level of free calcium in the granular cell cytosol plays a modulatory role in the control of apical membrane water and sodium permeability by vasopressin, and in the regulation of the basal rate of transepithelial sodium transport.

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.

Acidification of vasopressin-induced endosomes in toad urinary bladder

1994 ◽  
Vol 267 (1) ◽  
pp. F106-F113
Author(s):  
F. Emma ◽  
H. W. Harris ◽  
K. Strange
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Apical Membrane ◽  
Fluid Phase ◽  
Endocytic Pathway ◽  
Toad Urinary Bladder ◽  
Acidic Ph ◽  
Terminal Event ◽  
Ultimate Fate

It is well established that water channels (WC) are removed from the apical membrane of vasopressin-sensitive epithelia by endocytosis. The processing and the ultimate fate of endocytosed WC is, however, incompletely understood. In many cells, endosome acidification plays an important role in the processing and sorting of endocytosed proteins. Endosome acidification in the toad urinary bladder was therefore examined in vivo by fluorescence ratio video microscopy after induction of endocytosis by vasopressin removal and transepithelial water flow in the presence of the pH-sensitive fluid phase marker 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-dextran. Fifteen minutes after induction of endocytosis, the majority of endosomes had a neutral or slightly acidic pH. The number of acidic endosomes increased progressively with time. Two hours after endocytosis began, 98% of the endosomes had a pH < 6.0. Bafilomycin completely blocked endosome acidification, indicating that H+ transport is mediated by a vacuolar H(+)-adenosinetriphosphatase. Bafilomycin had no effect on transepithelial water flow in bladders repetitively stimulated by vasopressin. These findings, as well as the work of other investigators, suggest that if WC recycling occurs, it is not dependent on acidification of the endosomal compartment. Acidification of vasopressin-induced endosomes most likely represents a terminal event in the endocytic pathway.

Metabolic cost of sodium transport in toad urinary bladder

1977 ◽  
Vol 32 (1) ◽  
pp. 383-401 ◽  
Author(s):  
Pedro Labarca ◽  
Mitzy Canessa ◽  
Alexander Leaf
Keyword(s):  
Urinary Bladder ◽  
Sodium Transport ◽  
Metabolic Cost ◽  
Toad Urinary Bladder

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.

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