Concentrationo-dependence of nonelectrolyte permeability of toad bladder

1979 ◽  
Vol 48 (1) ◽  
pp. 21-42 ◽  
Author(s):  
Jing S. Chen ◽  
Mackenzie Walser
Keyword(s):  
Toad Bladder ◽  
Nonelectrolyte Permeability

Concentration-dependence of nonelectrolyte permeability of toad bladder

1980 ◽  
Vol 53 (3) ◽  
pp. 235-236
Author(s):  
Alvin Essig ◽  
M. Walser ◽  
J. S. Chen
Keyword(s):  
Concentration Dependence ◽  
Toad Bladder ◽  
Nonelectrolyte Permeability

OSMOTIC INHIBITION OF THE NATRIFERIC RESPONSE OF THE TOAD URINARY BLADDER TO VASOPRESSIN

1975 ◽  
Vol 67 (1) ◽  
pp. 119-125
Author(s):  
P. J. BENTLEY
Keyword(s):  
Urinary Bladder ◽  
Water Movement ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Electrical Potential Difference ◽  
Osmotic Gradient

SUMMARY The electrical potential difference and short-circuit current (scc, reflecting active transmural sodium transport) across the toad urinary bladder in vitro was unaffected by the presence of hypo-osmotic solutions bathing the mucosal (urinary) surface, providing that the transmural flow of water was small. Vasopressin increased the scc across the toad bladder (the natriferic response), but this stimulation was considerably reduced in the presence of a hypo-osmotic solution on the mucosal side, conditions under which water transfer across the membrane was also increased. This inhibition of the natriferic response did not depend on the direction of the water movement, for if the osmotic gradient was the opposite way to that which normally occurs, the response to vasopressin was still reduced. The natriferic response to cyclic AMP was also inhibited in the presence of an osmotic gradient. Aldosterone increased the scc and Na+ transport across the toad bladder but this response was not changed when an osmotic gradient was present. The physiological implications of these observations and the possible mechanisms involved are discussed.

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

scholarly journals Effects of butyrate on histone deacetylation and aldosterone-dependent Na+ transport in the toad bladder.

1983 ◽  
Vol 258 (5) ◽  
pp. 3388-3395
Author(s):  
A Truscello ◽  
K Geering ◽  
H P Gäggeler ◽  
B C Rossier
Keyword(s):  
Histone Deacetylation ◽  
Toad Bladder ◽  
Na Transport

Rat liver 11 beta-hydroxysteroid dehydrogenase complementary deoxyribonucleic acid encodes oxoreductase activity in a mineralocorticoid-responsive toad bladder cell line.

Endocrinology ◽  
1993 ◽  
Vol 132 (2) ◽  
pp. 612-619 ◽  
Author(s):  
H Duperrex ◽  
S Kenouch ◽  
H P Gaeggeler ◽  
J R Seckl ◽  
C R Edwards ◽  
...  
Keyword(s):  
Cell Line ◽  
Rat Liver ◽  
Deoxyribonucleic Acid ◽  
Hydroxysteroid Dehydrogenase ◽  
Toad Bladder ◽  
Bladder Cell ◽  
Complementary Deoxyribonucleic Acid

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.

Evidence for an apical membrane effect in the regulation of the hexose monophosphate shunt pathway in toad bladder studies with amiloride

1974 ◽  
Vol 332 (3) ◽  
pp. 350-357 ◽  
Author(s):  
Barbara Beckman ◽  
Beat Guertler ◽  
Rebecca Leaf ◽  
Patricia Witkum ◽  
Geoffrey W.G. Sharp
Keyword(s):  
Apical Membrane ◽  
Toad Bladder ◽  
Hexose Monophosphate ◽  
Shunt Pathway ◽  
Hexose Monophosphate Shunt ◽  
Membrane Effect

Quercetin enhances water transport in toad bladder

1981 ◽  
Vol 37 (7) ◽  
pp. 742-744 ◽  
Author(s):  
A. Grosso ◽  
R. C. de Sousa
Keyword(s):  
Water Transport ◽  
Toad Bladder

Cyclic 3',5'-AMP-Dependent Protein Kinase Activity in Toad Bladder Epithelium

1972 ◽  
Vol 140 (2) ◽  
pp. 657-660 ◽  
Author(s):  
M. A. Kirchberger ◽  
I. L. Schwartz ◽  
R. Walter
Keyword(s):  
Protein Kinase ◽  
Kinase Activity ◽  
Toad Bladder ◽  
Protein Kinase Activity ◽  
Bladder Epithelium ◽  
Dependent Protein Kinase ◽  
Dependent Protein
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