scholarly journals STIMULATION OF ACTIVE SODIUM TRANSPORT BY THE ISOLATED TOAD BLADDER WITH ALDOSTERONE IN VITRO*

1961 ◽  
Vol 40 (11) ◽  
pp. 2103-2110 ◽  
Author(s):  
Jean Crabbé
Keyword(s):  
Sodium Transport ◽  
Toad Bladder ◽  
Active Sodium ◽  
Active Sodium Transport ◽  
Stimulation Of

DECREASED EFFECTIVENESS OF ALDOSTERONE ON ACTIVE SODIUM TRANSPORT BY THE ISOLATED TOAD BLADDER IN THE PRESENCE OF OTHER STEROIDS

1964 ◽  
Vol 47 (3) ◽  
pp. 419-432 ◽  
Author(s):  
Jean Crabbé
Keyword(s):  
Active Transport ◽  
Sodium Transport ◽  
Concentration Ratio ◽  
Effective Concentration ◽  
Toad Bladder ◽  
Active Sodium ◽  
Active Sodium Transport ◽  
Hormonal Effect ◽  
Serosal Surface

ABSTRACT Aldosterone can stimulate the active transport of sodium by the isolated toad bladder in vitro. Corticosterone, cortisol, 17β-oestradiol and progesterone had no such effect despite incubation of the preparation with more than 100 times the smallest effective concentration of aldosterone. When the serosal surface of the membranes was exposed to 10 μg% d-aldosterone combined with 100 times this concentration of corticosterone, cortisol or progesterone, the stimulating action of aldosterone was reduced. Spirolactone SC 9420 failed to exert by itself a significant effect on the isolated toad bladder in vitro, but this compound blocked the stimulation by aldosterone of active sodium transport in vitro when present at concentrations 50 times those of aldosterone. When the concentration ratio was 10:1, a hormonal effect could be demonstrated, except at the highest concentration of the drug used.

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."

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.

Na-K activated adenosine triphosphatase and sodium transport in toad bladder

1964 ◽  
Vol 207 (5) ◽  
pp. 1005-1009 ◽  
Author(s):  
Sjoerd L. Bonting ◽  
Mel Rose Canady
Keyword(s):  
Cyclic Amp ◽  
Atpase Activity ◽  
Sodium Transport ◽  
Toad Bladder ◽  
Active Sodium ◽  
Direct Stimulation ◽  
Sodium Potassium ◽  
Dependent Atpase ◽  
Atpase System

The effect of several agents in vitro on sodium transport by the intact toad bladder and on sodium-potassium activated, magnesium-dependent ATPase (Na-K ATPase) activity has been examined in an attempt to elucidate the relationship between the agents, the Na-K ATPase system, and active sodium transport. Ouabain and erythrophleine inhibited sodium transport and Na-K ATPase activity, but had no effect on sodium-potassium independent, magnesium-dependent ATPase (Mg-ATPase) activity. Vasopressin, adenosine 3',5'-monophosphate (cyclic-AMP), and aldosterone had no effect on Na-K ATPase or Mg-ATPase activity. The results are compatible with the assumption that the Na-K ATPase system is closely related to the active sodium pump, and that ouabain and erythrophleine inhibit sodium transport by the bladder through inhibition of the Na-K ATPase system. The stimulatory effect on sodium transport of vasopressin, cyclic-AMP, and aldosterone is not due to direct stimulation of the Na-K ATPase system.

Stimulation of Sodium Transport Across the Isolated Toad Bladder by 1α-Hydroxycorticosterone from an Elasmobranch

1969 ◽  
Vol 26 (7) ◽  
pp. 1823-1835 ◽  
Author(s):  
A. S. Grimm ◽  
M. J. O'Halloran ◽  
D. R. Idler
Keyword(s):  
Seasonal Variation ◽  
Sodium Transport ◽  
Toad Bladder ◽  
Elasmobranch Fish ◽  
Peripheral Blood Plasma ◽  
Raja Radiata ◽  
Mineralocorticoid Activity ◽  
Relative Potencies ◽  
Stimulation Of

The mineralocorticoid activity of 1α-hydroxycorticosterone, an interrenal steroid in elasmobranch fish, was determined by the in vitro toad bladder bioassay. It stimulated the transport of sodium across the toad bladder at concentrations of 10−6, 10−7, and 10−8 M. The elasmobranch steroid had approximately 80% of the activity of d-aldosterone; it was slightly less active than aldosterone and corticosterone at the lower concentrations. Protein binding alone does not seem to explain the relative potencies of the two steroids. The concentrations of 1α-hydroxycorticosterone required to stimulate sodium transport across the toad bladder are comparable with those reported in the peripheral blood plasma of Raja radiata and R. ocellata. A seasonal variation in the number of positive responses was observed.

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