scholarly journals THE EFFECT OF CALCIUM WITHDRAWAL ON THE STRUCTURE AND FUNCTION OF THE TOAD BLADDER

1965 ◽  
Vol 25 (3) ◽  
pp. 195-209 ◽  
Author(s):  
Richard M. Hays ◽  
Bayla Singer ◽  
Sasha Malamed
Keyword(s):  
Epithelial Cells ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Structure And Function ◽  
Toad Bladder ◽  
Active Sodium ◽  
Bathing Medium ◽  
Active Sodium Transport ◽  
And Function

Previous reports have indicated that calcium is necessary to support active sodium transport by the toad bladder, and may be required as well in the action of vasopressin on both toad bladder and frog skin. The structure and function of the toad bladder has been studied in the absence of calcium, and a reinterpretation of the previous findings now appears possible. When calcium is withdrawn from the bathing medium, epithelial cells detach from one another and eventually from their supporting tissue. The short-circuit current (the conventional means of determining active sodium transport) falls to zero, and vasopressin fails to exert its usual effect on short-circuit current and water permeability. However, employing an indirect method for the estimation of sodium transport (oxygen consumption), it is possible to show that vasopressin exerts its usual effect on Qoo2 when sodium is present in the bathing medium. Hence, it appears that the epithelial cells maintain active sodium transport when calcium is rigorously excluded from the bathing medium, and continue to respond to vasopressin. The failure of conventional techniques to show this can be attributed to the structural alterations in the epithelial layer in the absence of calcium. These findings may provide a model for the physiologic action of calcium in epithelia such as the renal tubule.

Aldosterone-stimulated transmethylations are linked to sodium transport

1985 ◽  
Vol 248 (1) ◽  
pp. F43-F47 ◽  
Author(s):  
W. P. Wiesmann ◽  
J. P. Johnson ◽  
G. A. Miura ◽  
P. K. Chaing
Keyword(s):  
Epithelial Cells ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Methylation Inhibitor ◽  
In Cells

The effect of aldosterone (Aldo) on phospholipid (PL) biosynthesis in cultured toad bladder epithelial cells was studied in cells incubated with [1,2-14C]choline and [methyl-3H]methionine over a 5-h period. Aldo (10(-7) M) did not alter the uptake of either precursor but significantly stimulated the incorporation of both labels into phosphatidylcholine (PC), the only PL labeled. 3H labeling of PC increased 29% and 14C incorporation into PC increased 34% in cells exposed to Aldo. A similar 30% increase in protein carboxymethylation occurred in cells treated with Aldo. 3-Deazaadenosine (DZA), a methylation inhibitor, abolished the Aldo-stimulated increase in PC labeling from [3H]methionine. PC labeling from [1,2-14C]choline was not affected by DZA. Basal and Aldo-stimulated protein carboxy-methylation were inhibited by DZA. DZA (300 microM) caused a mild decrease in basal short-circuit current (ISC) but completely inhibited the ISC response to 10(-7) M Aldo. Inhibition was complete when DZA was added up to 2 h following exposure to Aldo, and was reversible. Cells previously exposed to Aldo showed a significant increase in ISC within 2 h following removal of DZA. We conclude that Aldo stimulates PL methylation, protein carboxymethylation, and turnover of PC from choline. Inhibition of methylation reactions coincides with the inhibition of ISC response to Aldo.

Anterior pituitary control of active sodium transport across frog skin

1961 ◽  
Vol 200 (3) ◽  
pp. 444-450 ◽  
Author(s):  
R. M. Myers ◽  
W. R. Bishop ◽  
B. T. Scheer
Keyword(s):  
Sodium Transport ◽  
Rana Pipiens ◽  
Sodium Current ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Anterior Lobe ◽  
Sodium Ion ◽  
Resting Potential ◽  
Active Sodium ◽  
Active Sodium Transport

Removal of the anterior lobe of the pituitary from the frog Rana pipiens is followed by an increase in the outflux of Na22 across the skin, which persists at least 4 months, and by a decrease in resting potential and sodium (‘short-circuit’) current, which persists no more than 3 weeks. The increased outflux is interpreted as resulting from increased permeability of the skin to sodium ion, and the decreased sodium current is interpreted as a decreased rate of active sodium transport. Either change is opposed by treatment with mammalian ACTH or with aldosterone. Effects of other hormones could not be established with certainty. The increased permeability of the skin to sodium appears to be associated with a decrease in the amount of a mucopolysaccharide in the dermis. The evidence suggests that the pituitary effects involve the interrenal bodies.

Aldosterone response in the turtle bladder is associated with an increase in ATP

1983 ◽  
Vol 245 (4) ◽  
pp. F512-F514
Author(s):  
N. Cortas ◽  
E. Abras ◽  
M. Walser
Keyword(s):  
Perchloric Acid ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Potential Difference ◽  
Freshwater Turtles ◽  
Active Sodium ◽  
Active Sodium Transport ◽  
Turtle Bladder

Urinary bladders from freshwater turtles, mounted as sacs, were stripped of their serosa and submucosa. This did not alter conductance. They were maintained in open circuit except for brief observation of short-circuit current (SCC) every 15 min. Potential difference (PD) averaged 68 +/- 14 mV and SCC 485 +/- 100 microA. Acetazolamide 10(-3) M increased SCC by 46 +/- 27 microA. Aldosterone 10(-7) M following acetazolamide resulted in a rise in SCC that began at about 75 min and reached a plateau between 3 and 5 h. SCC rose 127 +/- 15% compared with control bladder halves. ATP measured in perchloric acid extracts 5 h after addition of aldosterone increased by 33% (P less than 0.01) and (ATP)/(ADP) X (Pi) by 81% (P less than 0.01). These results support the view that the stimulatory effects of aldosterone on active sodium transport involve an increase in ATP and (ATP)/(ADP) X (Pi).

scholarly journals The Electrical Characteristics of Active Sodium Transport in the Toad Bladder

1963 ◽  
Vol 46 (3) ◽  
pp. 491-503 ◽  
Author(s):  
Howard S. Frazier ◽  
Alexander Leaf
Keyword(s):  
Sodium Transport ◽  
Short Circuit ◽  
Diffusion Potential ◽  
Toad Bladder ◽  
Chloride Diffusion ◽  
Active Sodium ◽  
High Potassium ◽  
Potential Step ◽  
Active Sodium Transport ◽  
Wide Range

The mechanism responsible for active sodium transport in the urinary bladder of the toad appears to be located at the serosal boundary of the epithelial cell layer of the bladder. Studies of the potential step observed at the serosal boundary in the open-circuited state were undertaken in an attempt to define the factors responsible for its production. Glass micropipettes were used to measure the serosal potential step in bladders exposed on the serosal side to solutions of high potassium or of high potassium and low chloride concentration. Observed potentials exceed the maximum values which would have been expected if the serosal potential step were a potassium or chloride diffusion potential. Measurements of net cation flux exclude the possibility of a diffusion potential at this border due to the passive movement of any anionic species. The observed independence of transbladder potential and short-circuit current from the pH of the serosal medium over a wide range of pH makes it unlikely that the observed serosal potential step is a hydrogen ion diffusion potential. We conclude that the active sodium transport mechanism in toad bladder is "electrogenic."

Tight monolayers of rat alveolar epithelial cells: bioelectric properties and active sodium transport

1989 ◽  
Vol 256 (3) ◽  
pp. C688-C693 ◽  
Author(s):  
J. M. Cheek ◽  
K. J. Kim ◽  
E. D. Crandall
Keyword(s):  
Epithelial Cells ◽  
Sodium Transport ◽  
Short Circuit ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial Cells ◽  
Active Sodium ◽  
Alveolar Epithelial ◽  
Active Sodium Transport ◽  
Complex Anatomy

Because the pulmonary alveolar epithelium separates air spaces from a fluid-filled compartment, it is expected that this barrier would be highly resistant to the flow of solutes and water. Investigation of alveolar epithelial resistance has been limited due to the complex anatomy of adult mammalian lung. Previous efforts to study isolated alveolar epithelium cultured on porous substrata yielded leaky monolayers. In this study, alveolar epithelial cells isolated from rat lungs and grown on tissue culture-treated Nucleopore filters resulted in tight monolayers with transepithelial resistance greater than 2,000 omega.cm2. Changes in bioelectric properties of these alveolar epithelial monolayers in response to ouabain, amiloride, and terbutaline are consistent with active sodium transport across a polarized barrier. 22Na flux measurements under short-circuit conditions directly confirm net transepithelial absorption of sodium by alveolar epithelial cells in the apical to basolateral direction, comparable to the observed short-circuit current (4.37 microA/cm2). The transport properties of these tight monolayers may be representative of the characteristics of the mammalian alveolar epithelial barrier in vivo.

11-Dehydrocorticosterone, a glucocorticoid metabolite, inhibits aldosterone action in toad bladder

1991 ◽  
Vol 261 (5) ◽  
pp. F873-F879 ◽  
Author(s):  
A. S. Brem ◽  
K. L. Matheson ◽  
J. L. Barnes ◽  
D. J. Morris
Keyword(s):  
Sodium Transport ◽  
Cell Layer ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Hydroxysteroid Dehydrogenase ◽  
Toad Bladder ◽  
Compound A ◽  
Dose Dependent Fashion ◽  
Epithelial Cell Layer ◽  
Dose Dependent

The enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) metabolizes glucocorticoid hormones and diminishes their ability to induce sodium transport. In these studies, we determined the location of this enzyme in toad bladder and assessed the biological role for its 11-dehydro end product. Employing a polyclonal antibody directed toward 11 beta-OHSD and immunofluorescence techniques, we located the enzyme in the epithelial cell layer of the toad bladder. Although corticosterone (10(-7) M) can partially suppress aldosterone (10(-7) M)-stimulated short-circuit current (SCC), a clear excess of corticosterone (10(-6) M) did not inhibit the aldosterone-induced induced (10(-8) M) rise in SCC (n = 6). The 11-dehydro product of corticosterone, 11-dehydrocorticosterone (compound A) added to the serosal bath suppressed aldosterone (10(-8) M) peak SCC (360 min) in a dose-dependent fashion reaching 46 +/- 5% of control values at 10(-5) M (n = 6; P less than 0.001). Compound A (10(-5) M) in the mucosal bath also was capable of partially inhibiting the peak aldosterone rise in SCC to 63 +/- 7% of control values with aldosterone at 10(-8) M (n = 6; P less than 0.01) and to 64 +/- 10% of control values with aldosterone at 10(-7) M (n = 9; P less than 0.01). Compound A alone at 10(-5) M did not have any effect on SCC. Isolated toad bladders were not able to transform compound A (at 10(-8) and 10(-5) M) back to corticosterone. Thus the 11-dehydro end product of 11 beta-OHSD (compound A) may play a biologic role by regulating a component of mineralocorticoid-induced sodium transport.

THE EFFECT OF VALINOMYCIN ON THE TOAD BLADDER: ANTAGONISM TO VASOPRESSIN AND ALDOSTERONE

1969 ◽  
Vol 45 (2) ◽  
pp. 287-295 ◽  
Author(s):  
P. J. BENTLEY
Keyword(s):  
Macrolide Antibiotic ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Water Transfer ◽  
Toad Bladder ◽  
Na Transport ◽  
Bathing Medium ◽  
Sodium Transfer ◽  
Sites Of Action ◽  
Subsequent Addition

SUMMARY The macrolide antibiotic valinomycin decreased short-circuit current (SCC, Na transport) across the isolated bladder of the toad. This effect was not overcome by increasing the K+ levels in the bathing medium or by the action of amphotericin B. The effects of vasopressin on both sodium and water transfer across the toad bladder were inhibited by valinomycin and the latter inhibition is non-competitive. The action of theophylline in increasing water transfer across the bladder was also inhibited. Cyclic AMP also increased water and Na+ transfer across the bladder but its action was not reduced by the macrolide. These results suggest that valinomycin inhibits adenyl cyclase. Aldosterone increases sodium transport across the toad bladder and this action was abolished by previous incubation of the tissue with the macrolide. Once the steroid-induced effect had been established subsequent addition of valinomycin did not alter the sodium transfer. Valinomycin thus appears to have several sites of action on the toad bladder.

Effects of EGF on alveolar epithelial junctional permeability and active sodium transport

1996 ◽  
Vol 270 (4) ◽  
pp. L559-L565 ◽  
Author(s):  
Z. Borok ◽  
A. Hami ◽  
S. I. Danto ◽  
R. L. Lubman ◽  
K. J. Kim ◽  
...  
Keyword(s):  
Sodium Transport ◽  
Egf Receptor ◽  
Alveolar Epithelial Cell ◽  
Short Circuit ◽  
Specific Inhibitor ◽  
Egf Receptors ◽  
Active Sodium ◽  
Alveolar Epithelial ◽  
Active Sodium Transport ◽  
Junctional Permeability

We evaluated the effects of epidermal growth factor (EGF) on transepithelial resistance (Rt) and active ion transport by alveolar epithelial cell (AEC) monolayers on tissue culture-treated polycarbonate filters. Rat type II cells were cultured in completely defined serum-free medium (MDSF) or MDSF supplemented with EGF. The addition of EGF from either day 0 (chronic) or day 4 (subacute) resulted in significant increases in Rt and short-circuit current (ISC) on day 5. After subacute exposure, these effects were delayed in onset by 6-12 h and sustained for > 24 h. Basolateral (but not apical) EGF was responsible for these effects, which were prevented by preincubation with tyrphostin RG-50864, a reversible specific inhibitor of the EGF receptor tyrosine kinase. ISC decreased, with a sensitivity to apical inhibitors of sodium transport in the order benzamil > amiloride > 5-(N-ethyl-N-isopropyl) amiloride in MDSF +/- EGF, and was completely inhibited by the addition of basolateral ouabain. Net sodium flux and Na+, K+ -ATPase activity both increased approximately 50% in the presence of EGF. These results indicate that 1) EGF decreases tight junctional permeability and increases active sodium transport by AEC monolayers via basolaterally located EGF receptors, and 2) the pathways for AEC sodium entry and exit (+/- EGF) are apical high amiloride affinity sodium channels and basolateral sodium pumps.

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