Effect of omitting potassium from serosal medium on the sodium transport across toad bladder

1969 ◽  
Vol 31 (4) ◽  
pp. 547-554 ◽  
Author(s):  
R.S Snart ◽  
T Dalton ◽  
D.W Wright
Keyword(s):  
Sodium Transport ◽  
Toad Bladder

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.

scholarly journals Effect of Tetrodotoxin on the Sodium Transport of the Toad Bladder

1967 ◽  
Vol 43 (5) ◽  
pp. 404-406 ◽  
Author(s):  
Fumiaki MARUMO ◽  
Yasushi ASANO ◽  
Takuo SASAOKA ◽  
Shozo KOSHIKAWA
Keyword(s):  
Sodium Transport ◽  
Toad Bladder

scholarly journals Sodium Transport in the Toad Bladder

1971 ◽  
Vol 28 (5_suppl_2) ◽  
Author(s):  
HOWARD S. FRAZIER
Keyword(s):  
Urinary Bladder ◽  
Sodium Transport ◽  
Mode Of Action ◽  
Renal Tubule ◽  
Alternative Hypothesis ◽  
Toad Bladder ◽  
Second Step ◽  
Epithelial Layer ◽  
Granular Cells ◽  
Simple Alternative

The isolated urinary bladder of the toad transports sodium actively across its epithelial layer and responds to the hormones vasopressin and aldosterone, properties which make it a useful model for the study of certain functions of the renal tubule. Sodium transport in the granular cells of the bladder is thought to involve first an energetically passive but selective entry step at the mucosal surface, the rate of which is increased after vasopressin administration. The second step in transport is considered to be active extrusion of the ion across the serosal boundary of the cell. Recent evidence concerning the cellular pool of sodium and the site and mode of action of vasopressin suggests that this description is at best incomplete. No equally simple alternative hypothesis for the organization of sodium transport in this system is available at present.

Effect of sodium transport inhibition on active phosphate transport by toad bladder

1978 ◽  
Vol 41 (4) ◽  
pp. 323-328 ◽  
Author(s):  
Billy B. Sellers ◽  
Julia A. Hall ◽  
Stanley A. Mendoza
Keyword(s):  
Sodium Transport ◽  
Phosphate Transport ◽  
Toad Bladder ◽  
Transport Inhibition

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.

Refractoriness of toad bladder to stimulation of sodium transport

1972 ◽  
Vol 223 (1) ◽  
pp. 104-109 ◽  
Author(s):  
SA Mendoza ◽  
F Murad ◽  
JS Handler ◽  
J Orloff
Keyword(s):  
Sodium Transport ◽  
Toad Bladder ◽  
Stimulation Of

scholarly journals The Site of the Stimulatory Action of Vasopressin on Sodium Transport in Toad Bladder

1968 ◽  
Vol 51 (5) ◽  
pp. 589-605 ◽  
Author(s):  
Mortimer M. Civan ◽  
Howard S. Frazier
Keyword(s):  
Sodium Transport ◽  
Direct Evidence ◽  
Ionic Mobility ◽  
Toad Bladder ◽  
Permeability Barrier ◽  
Total Resistance ◽  
Stimulatory Action ◽  
Resistance Change ◽  
Site Of Action ◽  
Mucosal Side

Vasopressin increases the net transport of sodium across the isolated urinary bladder of the toad by increasing the mobility of sodium ion within the tissue. This change is reflected in a decreased DC resistance of the bladder; identification of the permeability barrier which is affected localizes the site of action of vasopressin on sodium transport. Cells of the epithelial layer were impaled from the mucosal side with glass micropipettes while current pulses were passed through the bladder. The resulting voltage deflections across the bladder and between the micropipette and mucosal reference solution were proportional to the resistance across the entire bladder and across the mucosal or apical permeability barrier, respectively. The position of the exploring micropipette was not changed and vasopressin was added to the serosal medium. In 10 successful impalements, the apical permeability barrier contributed 54% of the initial total transbladder resistance, but 98% of the total resistance change following vasopressin occurred at this site. This finding provides direct evidence that vasopressin acts to increase ionic mobility selectively across the apical permeability barrier of the transporting cells of the toad bladder.

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