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.

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 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.

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.

MECHANISM OF ACTION OF NEUROHYPOPHYSIAL HORMONES: ACTIONS OF MANGANESE AND ZINC ON THE PERMEABILITY OF THE TOAD BLADDER

1967 ◽  
Vol 39 (4) ◽  
pp. 493-506 ◽  
Author(s):  
P. J. BENTLEY
Keyword(s):  
Urinary Bladder ◽  
Cyclic Amp ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Antagonistic Effect ◽  
Mucosal Surface ◽  
Toad Urinary Bladder ◽  
Competitive Antagonist ◽  
Osmotic Permeability

SUMMARY The short-circuit current (SCC, sodium transport) across the isolated toad urinary bladder was increased by the presence of 10−4m-Mn2+ at the serosal but not at the mucosal surface. Magnesium did not have this effect. Zinc (10−4m) decreased the SCC. Neither Mn2+ nor Zn2+ altered the SCC at a concentration of 10−5m. Oxytocin stimulated sodium transport across the bladder and this response was reduced by 10−4 but not by 10−5m-Mn2+. Zinc (10−5m) nearly abolished the effect of oxytocin. Normal osmotic permeability of the bladder to water was unaffected by 10−4m-Mn2+ or Zn2+. Oxytocin increased the osmotic permeability of the bladder to water and this response was strongly inhibited by 10−4 and 10−5m-Mn2+ at the serosal but not at the mucosal surface. Magnesium did not have this effect. Zinc (10−4 to 10−6m) similarly reduced this effect of oxytocin but at a concentration of 10−4m also acted at the mucosal surface. The antagonistic effect of Mn2+ on the action of oxytocin on osmotic permeability was not reversible and was non-competitive. Zn2+ was also found to be a non-competitive antagonist of oxytocin but the antagonism was reversible. The increase in osmotic permeability of the bladder to water by the addition of cyclic AMP was unaffected by Mn2+. In contrast Zn2+ reduced the effects of cyclic AMP on both osmotic permeability and SCC. It is suggested that Mn2+ uncouples processes linking the interaction of oxytocin with the formation of cyclic AMP in the bladder while Zn2+ acts at a stage subsequent to the formation of the nucleotide, possibly on the effector mechanisms themselves.

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 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.

Stimulation of sodium transport in toad bladder by acidification of mucosal medium

1964 ◽  
Vol 207 (3) ◽  
pp. 547-552 ◽  
Author(s):  
Alexander Leaf ◽  
Albert Keller ◽  
Eleanor F. Dempsey
Keyword(s):  
Urinary Bladder ◽  
Sodium Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Ph Optimum ◽  
Tissue Ph ◽  
Mucosal Acidification ◽  
Sodium Flux ◽  
Stimulation Of

The short-circuit current, sodium flux, and electrical potential across the isolated urinary bladder of the toad were stimulated by acidification of the medium bathing the mucosal or urinary surface of the bladder. By contrast the transport of chloride, potassium, urea, and water across the bladder was unaffected by similar acidification. The pH optimum for this action was approximately 5.5. The tissue pH, as determined by the distribution of DMO-C14, was not detectably affected by mucosal acidification.

Inhibition of short-circuit current in toad urinary bladder by inhibitors of glandular kallikrein

1980 ◽  
Vol 239 (5) ◽  
pp. F459-F465 ◽  
Author(s):  
G. G. Orce ◽  
G. A. Castillo ◽  
H. S. Margolius
Keyword(s):  
Urinary Bladder ◽  
Short Circuit ◽  
Serine Proteinase ◽  
Protein S ◽  
Short Circuit Current ◽  
Reversible Inhibitor ◽  
Toad Urinary Bladder ◽  
Irreversible Inhibitor ◽  
Glandular Kallikrein ◽  
Renal Kallikrein

Aprotinin, a reversible inhibitor, and D-Phe-Phe-Arg-chloromethyl ketone (DPPA), an irreversible inhibitor of mammalian glandular kallikreins, decreased short-circuit current (SCC) in the isolated toad urinary bladder. Both were more potent and rapidly acting on the mucosal than serosal surface. The maximal inhibition in basal SCC was 29% for aprotinin and 41% for DPPA at concentrations of 7.0 X 10(-6) and 1.0 X 10(-5) M, respectively. SCC inhibition with mucosal aprotinin was reversed by rinsing, whereas inhibition with mucosal DPPA was not reversible. The presence of either agent in the mucosal bath inhibited the SCC increase to serosal vasopressin, but neither modified this response when present in the serosal bath. Neither agent affected basal or vasopressin-stimulated osmotic water permeability. Aprotinin did not prevent aldosterone-induced increases in SCC. Soybean trypsin inhibitor, an inhibitor of plasma but not glandular kallikrein, did not affect SCC. We postulate that these inhibitors of mammalian glandular kallikreins act upon some accessible serine proteinase(s) to reduce short-circuit current. This protein(s) might be an amphibian homologue of mammalian renal kallikrein.

Dependence of the driving force of the sodium pump on rate of transport

1977 ◽  
Vol 232 (5) ◽  
pp. F448-F454
Author(s):  
Peter U. Feig ◽  
Gayle D. Wetzel ◽  
Howard S. Frazier
Keyword(s):  
Active Transport ◽  
Sodium Transport ◽  
Driving Force ◽  
Sodium Pump ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Base Line ◽  
Chemical Gradient ◽  
Electrical Analogue ◽  
Additional Support

The driving force for active transport of Na+ in the isolated toad bladder, ENa, was measured as the reciprocal slope of the change in conductance with change in short-circuit current after stimulation with antidiuretic hormone. The base-line short-circuit current was altered by change in ambient Na+ concentration or addition of amiloride, maneuvers which alter availability of Na+ at the site of active transport. In the absence of a chemical gradient for Na+ across the bladder, ENa was found to be inversely related to the rate of Na+ transport, a finding incompatible with the simple electrical analogue that has been proposed for the system. The results provide additional support for the view that ENa measured in this way has both energetic and kinetic components. membrane transport; active transport; sodium transport; ENa Submitted on April 23, 1976

Tetracycline-induced inhibition of Na+ transport in the toad urinary bladder

1978 ◽  
Vol 235 (4) ◽  
pp. F359-F366 ◽  
Author(s):  
J. Guzzo ◽  
M. Cox ◽  
A. B. Kelley ◽  
I. Singer
Keyword(s):  
Urinary Bladder ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Lipid Solubility ◽  
Toad Urinary Bladder ◽  
Na Transport ◽  
Ussing Chambers ◽  
Incubation Periods ◽  
Active Conductance ◽  
Drug Protein Binding

The effects of three tetracyclines, demethylchlortetracycline (DMC), minocycline (MNC), and oxytetracycline (OTC), on Na+ transport (measured as short-circuit current) were examined in toad urinary bladders mounted in modified Ussing chambers. During a 1-h incubation period serosal DMC (but not MNC or OTC) inhibited basal Na+ transport, whereas MNC (but not DMC or OTC) inhibited ADH-stimulated Na+ transport. MNC also inhibited cyclic AMP-stimulated Na+ transport. During longer incubation periods all three drugs inhibited basal Na+ transport. The DMC-induced inhibition of basal Na+ transport and the MNC-induced inhibition of ADH-stimulated Na+ transport were paralleled by an inhibition of the active conductance of the bladders. Thus, although all three drugs inhibit basal Na+ transport, only MNC inhibits ADH-stimulated Na+ transport. This effect does not correlate with the known effects of the tetracyclines on ADH-stimulated water flow or with drug-protein binding, and may be related to the greater lipid solubility of MNC.

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