Cytosolic calcium and the action of vasopressin in toad urinary bladder

1987 ◽  
Vol 252 (6) ◽  
pp. F1028-F1041
Author(s):  
A. Taylor ◽  
E. Eich ◽  
M. Pearl ◽  
A. S. Brem ◽  
E. Q. Peeper
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Sodium Transport ◽  
Short Circuit ◽  
Exchange Process ◽  
Cytosolic Calcium ◽  
Free Calcium ◽  
Toad Urinary Bladder ◽  
Low Sodium ◽  
Transepithelial Sodium Transport

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.

Hormone effects on transport in cultured epithelia with high electrical resistance

1981 ◽  
Vol 240 (3) ◽  
pp. C103-C105 ◽  
Author(s):  
J. S. Handler ◽  
F. M. Perkins ◽  
J. P. Johnson
Keyword(s):  
Urinary Bladder ◽  
Cell Lines ◽  
Sodium Transport ◽  
Time Course ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Transepithelial Resistance ◽  
Striking Difference ◽  
Toad Urinary Bladder ◽  
Hormone Effects

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.

Effect of carbenoxolone on glucocorticoid metabolism and Na transport in toad bladder

1989 ◽  
Vol 257 (4) ◽  
pp. F700-F704
Author(s):  
A. S. Brem ◽  
K. L. Matheson ◽  
T. Conca ◽  
D. J. Morris
Keyword(s):  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Water Soluble ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Base Line ◽  
Target Tissue ◽  
Glucocorticoid Metabolism ◽  
Transepithelial Sodium Transport

In humans, diminished 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) enzyme activity has been associated with sodium retention and hypertension. These studies show that the toad bladder, another target tissue epithelium displaying steroid-induced sodium transport, possesses the enzyme 11 beta-OHSD. The toad urinary bladder rapidly transformed corticosterone (3 x 10(-8) M) (50% by 10 min and 90% by 180 min) with 11-dehydrocorticosterone being the major metabolite. The 11-dehydrocorticosterone produced reached an apparent plateau when the tissue incubations were repeated with higher concentrations of corticosterone (10(-7) and 10(-6) M). Carbenoxolone sodium (2.5 x 10(-5) M), a water soluble derivative of glycyrrhetinic acid, markedly inhibited the metabolism of corticosterone (3 x 10(-8) M) to 11-dehydrocorticosterone similar to previous observations in the mammalian kidney. Carbenoxolone sodium (2.5 x 10(-5) M) did not significantly affect short-circuit current (SCC) in toad bladders when added to either the serosal or mucosal bath. However, when carbenoxolone sodium was added to the mucosal bath and 60 min later corticosterone 10(-6) M was placed in the serosal bath, bladders generated a SCC 2.07 +/- 0.17 (mean +/- SE) times above base line at 360 min compared with 1.48 +/- 0.11 in bladders exposed to corticosterone alone (P less than 0.02). In parallel experiments, carbenoxolone sodium in the mucosal bath enhanced the rise in SCC induced by cortisol 10(-6) M; 1.66 +/- 0.16 times above base line at 360 min compared with 1.07 +/- 0.14 with cortisol alone (P less than 0.02). We conclude that the toad bladder contains 11 beta-OHSD and inhibition of this enzyme with carbenoxolone sodium is associated with amplification of glucocorticoid-induced transepithelial sodium transport in this tissue. However, since the quantity of 11-dehydro-product produced appears to be limited, other factors in addition to inhibition of 11 beta-OHSD may play a role in this amplification of sodium transport.

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
Keyword(s):  
Urinary Bladder ◽  
Sodium Transport ◽  
Cardiac Glycoside ◽  
Rate Coefficient ◽  
Potential Gradient ◽  
Electrochemical Potential ◽  
Toad Urinary Bladder ◽  
Transepithelial Sodium Transport

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.

Effect of stretch on passive transport in toad urinary bladder

1976 ◽  
Vol 230 (6) ◽  
pp. 1722-1729 ◽  
Author(s):  
PD Lief ◽  
BF Mutz ◽  
N Bank
Keyword(s):  
Urinary Bladder ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Urinary Bladder ◽  
Internal Volume ◽  
Acute Changes ◽  
Large Stretch ◽  
Intercellular Pathway ◽  
Total Tissue

In order to gain further information about the effect of stretch on the urinary bladder of the toad, transepithelial movement of radioactive sucrose, chloride, and urea was measured across bladder sacs during acute changes in the internal volume. Short-circuit current (SCC) and total tissue conductance (Kt) were also measured in each experiment. It was found that sudden large increases or smaller graded increases in volume resulted in a consistent fall in the tracer permeability (P*) of all three isotopes. However, this fall was due entirely to the larger area term in the calculation of P* rather than any real change in isotope movement. When total diffusion (TD) of each isotope was calculated by a method that eliminated the changes in surface area, it was apparent that stretch produced no significant effects on the transepithelial movement of any of these three molecules. Large stretch also resulted in parallel increases in SCC and Kt in most bladders. We conclude from these observations that the intercellular pathway for sucrose and chloride and the transcellular pathway for urea are unaltered by degrees of stretch that enhance SCC and sodium transport. By inference, the observed increases in Kt appear to represent changes in specific active pathway conductance (Ka), and may relate importantly to the changes in sodium transport.

Possible role of cytosolic calcium and Na-Ca exchange in regulation of transepithelial sodium transport

1979 ◽  
Vol 236 (6) ◽  
pp. F505-F512 ◽  
Author(s):  
A. Taylor ◽  
E. E. Windhager
Keyword(s):  
Sodium Transport ◽  
Calcium Ion ◽  
Critical Role ◽  
Cytosolic Calcium ◽  
Feedback Mechanism ◽  
Toad Urinary Bladder ◽  
Renal Tubules ◽  
Apical Surface ◽  
Negative Feedback Mechanism ◽  
Transepithelial Sodium Transport

Emerging evidence in a number of different epithelia suggests that changes in cytosolic calcium ion levels play a critical role in the regulation of transepithelial sodium transport. Maneuvers believed to raise cytosolic calcium ion activity lead to an inhibition of net sodium transport in toad urinary bladder, frog skin, and isolated perfused proximal renal tubules. Regulation of the level of ionized calcium in the cytosol of the epithelial cells appears to involve a process of coupled Na-Ca exchange across the basolateral plasma membrane, energized, at least in part, by the sodium gradient. It is suggested that changes in cytosolic calcium ion levels, secondary to changes in Na-Ca exchange, in turn dependent in part on the activity of the sodium pump, constitute a link in a negative feedback mechanism. Through such a feedback mechanism, the rate of entry of sodium into the cell across the apical surface may be kept in step with its rate of extrusion across the basolateral surface.

Effect of insulin on short-circuit current and sodium transport across toad urinary bladder

1965 ◽  
Vol 209 (4) ◽  
pp. 819-824 ◽  
Author(s):  
Francisco C. Herrera
Keyword(s):  
Urinary Bladder ◽  
Sodium Transport ◽  
Rate Coefficient ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Mucosal Surface ◽  
Rate Coefficients ◽  
Toad Urinary Bladder ◽  
Bladder Epithelium ◽  
Stimulation Of

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.

Polycations reduce vasopressin-induced water flow by endocytic removal of water channels

1986 ◽  
Vol 250 (5) ◽  
pp. C729-C737 ◽  
Author(s):  
R. Beauwens ◽  
G. te Kronnie ◽  
J. Snauwaert ◽  
P. A. in't Veld
Keyword(s):  
Urinary Bladder ◽  
Water Flow ◽  
Sodium Channels ◽  
Sodium Transport ◽  
Water Channels ◽  
Toad Urinary Bladder ◽  
Cationized Ferritin ◽  
Ultrastructural Studies ◽  
Urea Permeability ◽  
Luminal Cells

Several polycations added to the luminal solution were found to inhibit the vasopressin (ADH)-induced water flow in toad urinary bladder but not the ADH-induced increase in sodium transport or in urea permeability. Ultrastructural studies were conducted to evaluate the uptake of cationized ferritin. It was found that endocytosis of cationized ferritin by luminal cells was strikingly enhanced on exposure to ADH; this increased endocytosis was concomitant with inhibition of transepithelial ADH-induced water flow. Various maneuvers preventing endocytosis were also found to counteract the polycation-induced inhibition of the ADH effect. It is suggested that polycations are endocytosed in vesicles whose walls contain the water channels but not the urea or sodium channels.

Effect of magnesium on sodium transport in toad urinary bladder

1978 ◽  
Vol 234 (3) ◽  
pp. F192-F198
Author(s):  
A. J. Aguilera ◽  
K. L. Kirk ◽  
G. F. DiBona
Keyword(s):  
Urinary Bladder ◽  
Voltage Clamp ◽  
Sodium Transport ◽  
Sodium Pump ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Urinary Bladder ◽  
Electrical Parameters ◽  
Effect Analysis ◽  
Mg Substitution

Voltage-clamp techniques were employed to examine the effect of magnesium (Mg) on sodium transport in the isolated urinary bladder of the Dominican toad. Substitution of 1 mM Mg had no effect, but 3-mM Mg substitution resulted in a reversible increase in short-circuit current (27%) and potential difference (19%) and decrease in transepithelial resistance (14%); no greater effect was seen with 5- or 10-mM Mg substitution. The effect was produced by mucosal or mucosal and serosal Mg substitution; serosal Mg substitution was without effect. Analysis of electrical parameters disclosed that magnesium increased net sodium transport via an effect on the sodium pump.

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