scholarly journals Action of ouabain on sodium transport in toad urinary bladder, Evidence for two pathways for sodium entry.

1975 ◽  
Vol 65 (4) ◽  
pp. 503-514 ◽  
Author(s):  
A L Finn

The cardiac glycoside ouabain inhibits transepithelial sodium transport in the toad urinary bladder. It is shown that this drug reduces the rate coefficient for sodium exit at the serosal pump site. In addition, ouabain inhibits entry across the mucosal border whenever the electrochemical potential gradient for sodium is made less favorable. The data are interpreted as indicating the existence of two separate pathways for sodium entry, one of which is ouabain inhibitable.

1965 ◽  
Vol 209 (4) ◽  
pp. 819-824 ◽  
Author(s):  
Francisco C. Herrera

The effect of insulin on short-circuit current and on the sodium transport system of the toad bladder has been examined. The rate coefficients for sodium movements across the mucosal and serosal barriers of the bladder epithelium were studied by observing the approach to a steady value of the flux of Na22 across the bladder. Insulin added to the solutions bathing both surfaces of the bladder causes a marked increase in short-circuit current. A smaller effect may also be elicited by adding the hormone to either the serosal or the mucosal bathing media. Insulin causes an important increase in the rate coefficient for sodium movement from the cells to the serosal solution with no significant change in the rate co-efficients for sodium movement across the mucosal surface of the epithelial cells. The results indicate that the action of insulin is the result of a stimulation of the active transport step at the serosal surface of the cells. Insulin does not appear to modify the permeability to sodium of the mucosal surface.


1987 ◽  
Vol 252 (6) ◽  
pp. F1028-F1041
Author(s):  
A. Taylor ◽  
E. Eich ◽  
M. Pearl ◽  
A. S. Brem ◽  
E. Q. Peeper

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.


1977 ◽  
Vol 32 (1) ◽  
pp. 383-401 ◽  
Author(s):  
Pedro Labarca ◽  
Mitzy Canessa ◽  
Alexander Leaf

1981 ◽  
Vol 240 (3) ◽  
pp. C103-C105 ◽  
Author(s):  
J. S. Handler ◽  
F. M. Perkins ◽  
J. P. Johnson

Three continuous lines of amphibian epithelial cells form epithelia with a high transepithelial resistance (greater than 4,000 omega . cm2) in culture. The cell lines are TB-M and TB-6c, derived from the urinary bladder of Bufo marinus, and A6, derived from the kidney of Xenopus laevis. Short-circuit current is equivalent to net mucosa-to-serosa sodium transport in two cell lines and slightly exceeds sodium transport in epithelia formed by TB-6c cells. None of the cell lines has an adenylate cyclase response or a transport or permeability response to vasopressin. Water permeability is low in all three cell lines and is not affected by adenosine 3',5–-cyclic monophosphate (cAMP). In the three lines of cells, cAMP and aldosterone each increases short-circuit current with a time course similar to that seen in naturally occurring epithelia. In contrast to the toad urinary bladder and epithelia of line TB-M in which the aldosterone stimulation of short-circuit current is associated with a fall in transepithelial resistance, there is no change in resistance across epithelia of lines TB-6c and A6. There is also a striking difference in the sensitivity of the three lines to inhibition of short-circuit current by amiloride.


1974 ◽  
Vol 17 (1) ◽  
pp. 253-262 ◽  
Author(s):  
Arthur L. Finn ◽  
Susan A. Hutton

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