scholarly journals EFFECTS OF CYTOCHALASIN B ON THE RESPONSE OF TOAD URINARY BLADDER TO VASOPRESSIN

1974 ◽  
Vol 63 (3) ◽  
pp. 986-997 ◽  
Author(s):  
Walter L. Davis ◽  
David B. P. Goodman ◽  
Richard J. Schuster ◽  
Howard Rasmussen ◽  
James H. Martin
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Morphological Study ◽  
Cytochalasin B ◽  
Water Movement ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Osmotic Response

A combined physiological and morphological study of the effects of cytochalasin B (CB) on the toad urinary bladder has been carried out. CB inhibits the hydro-osmotic response to vasopressin without altering basal water permeability or diffusion, or the increase in 3H2O diffusion observed after hormone addition. Although CB increases [22Na]-, [36Cl]-, and [14C]urea fluxes, and decreases transepithelial potential, no alteration in basal short-circuit current, the vasopressin-induced increase in this parameter, or [14C]inulin permeability occurs. In the absence of hormone, CB does not markedly alter the structure of the toad bladder. However, in the presence of vasopressin, CB induces the formation of large intracellular vacuoles. These results suggest a possible coupling of solute and water movement across the tissue.

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.

EFFECTS OF CADMIUM ON THE HYDRO-OSMOTIC AND NATRIFERIC RESPONSES OF THE TOAD BLADDER TO VASOPRESSIN

1975 ◽  
Vol 66 (2) ◽  
pp. 273-278 ◽  
Author(s):  
P. J. BENTLEY ◽  
T. YORIO ◽  
L. FLEISHER
Keyword(s):  
Urinary Bladder ◽  
Cyclic Amp ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Bathing Solution ◽  
Serosal Side ◽  
Osmotic Effect ◽  
Osmotic Response

SUMMARY Cadmium, 10−3 mol/l on the mucosal or 10−5 mol/l on the serosal side of the toad urinary bladder, inhibits the hydro-osmotic effect of vasopressin. This inhibition is irreversible. The osmotic transfer of water in the absence of vasopressin was unaffected by the presence of the Cd2+. The hydro-osmotic response to cyclic AMP was also reduced by the Cd2+, but the response due to hypertonicity of the serosal bathing solution was unaffected. The short-circuit current (reflecting active transmural Na+ transport) was inhibited by 10−3 mol Cd2+/1 on the serosa, but was increased by 10−3 mol/l at the mucosa or 10−4 mol/l at the serosa. The natriferic response of the bladder to vasopressin was unaffected when Cd2+ was present under conditions that inhibited the hydro-osmotic response, further emphasizing that separate effector mechanisms may be involved for each effect.

Anion transport inhibitors: effects on water and sodium transport in the toad urinary bladder

1985 ◽  
Vol 248 (4) ◽  
pp. F594-F601 ◽  
Author(s):  
A. S. Brem ◽  
E. Eich ◽  
M. Pearl ◽  
A. Taylor
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Cyclic Nucleotide ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Anion Transport ◽  
Toad Urinary Bladder ◽  
Dependent Manner ◽  
Bathing Medium ◽  
Transport Inhibitors

Acidification of the medium bathing the serosal surface of the toad urinary bladder results in impairment of the water permeability response to vasopressin. The magnitude of the hydrosmotic response to a maximal concentration of either vasopressin or the cyclic nucleotide analogue 8-(p-chlorophenylthio)-cyclic 3',5'-adenosine monophosphate (C1PhS-cAMP) was progressively reduced when serosal bath pH was decreased from 8.5 to 6.5. The disulfonic stilbenes SITS and DIDS and the diuretic furosemide, agents known to interfere with anion transport and with the regulation of intracellular pH in other tissues, inhibited the water flow response to vasopressin and C1PhS-cAMP in a pH-dependent manner when added to the serosal bathing medium. Inhibition of the hydrosmotic response to 10(-5) M C1PhS-cAMP was estimated to be half-maximal at 1.5 X 10(-4) M SITS, 2 X 10(-5) M DIDS, and 1 X 10(-5) M furosemide. The degree of inhibition induced by the anion transport inhibitors varied inversely with the concentration of exogenous cyclic nucleotide. SITS, DIDS, and furosemide had no effect on either basal or vasopressin-stimulated short-circuit current at serosal pH 8.5; all three agents inhibited basal short-circuit current at pH 7.1 but had no effect on the natriferic response to vasopressin. These results are consistent with the view that changes in intracellular hydrogen ion and/or anion concentration can selectively inhibit the increase in water permeability elicited by vasopressin at a step(s) distal to the generation of cAMP.

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.

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.

Effects of serosal hypertonicity on water permeability in toad urinary bladder

1990 ◽  
Vol 258 (5) ◽  
pp. C871-C878 ◽  
Author(s):  
W. A. Kachadorian ◽  
K. R. Spring ◽  
N. L. Shinowara ◽  
J. Muller ◽  
T. A. Palaia ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Water Permeability ◽  
Water Movement ◽  
Granular Cell ◽  
Toad Urinary Bladder ◽  
Morphological Examination ◽  
Tissue Water ◽  
Coated Pits ◽  
Thin Sections ◽  
Luminal Membrane

We studied in toad urinary bladder the effects of serosal hypertonicity on tissue water permeability, granular cell luminal membrane water permeability, and granular cell luminal membrane particle aggregates and compared them with effects of antidiuretic hormone (ADH). In tissues challenged by a hypertonic (447 mosmol/kgH2O) serosal bath, luminal membrane aggregates were structurally similar to those caused by ADH. The tissue water permeability increase induced by serosal hypertonicity was much less than that caused by a maximally stimulating concentration of ADH on tissue in isotonic serosal baths with approximately the same transmural gradient. The difference is explained not only by a reduced incidence of luminal membrane aggregates but also by an increased resistance to water movement at a postluminal membrane site. Measurements of luminal membrane water permeability showed a close correlation with luminal membrane aggregate frequency, indicating that the calculated permeability of an individual aggregate was a constant. Thus the relation of luminal membrane aggregates to tissue osmotic permeability is modified by serosal hypertonicity. Morphological examination of these tissues suggested that luminal membrane aggregates may be less stable in the absence of hormone. This was evident by the proportionally greater number of structures interpreted as aggregates captured in the process of disassembly ("patches"). Membrane depressions containing intramembrane particles ("craters") were also observed. They corresponded in terms of frequency and size to coated pits as seen in thin sections.

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.

Effect of brefeldin A on ADH-induced transport responses of toad bladder

1994 ◽  
Vol 266 (4) ◽  
pp. C1069-C1076 ◽  
Author(s):  
K. Weng ◽  
J. B. Wade
Keyword(s):  
Water Permeability ◽  
Short Circuit ◽  
Brefeldin A ◽  
Membrane Traffic ◽  
Short Circuit Current ◽  
Toad Urinary Bladder ◽  
Membrane Biogenesis ◽  
Na Transport ◽  
Stimulation Of

We have used brefeldin A (BFA) to examine the role of membrane traffic in the short-circuit current (ISC) and water permeability responses of the toad urinary bladder. BFA treatment of 1 or 5 micrograms/ml had a complex effect on the response of the ISC to antidiuretic hormone (ADH) or forskolin stimulation. Although the responses to initial challenges by ADH were not impaired by BFA, subsequent ISC responses were progressively reduced. Similarly, while the response to an initial challenge by forskolin was modestly reduced by BFA, subsequent responses were markedly reduced. Inhibition of protein synthesis with cycloheximide (CHM) affected ISC responses similarly. Neither BFA nor CHM had an effect on water permeability responses. These observations show that although the membrane traffic responsible for the water permeability response is insensitive to inhibition by BFA or CHM, the stimulation of Na+ transport becomes increasingly sensitive to these inhibitors with successive challenges by ADH or forskolin. Although initial increases in Na+ transport utilize preexisting components, subsequent responses appear to require an intact system for membrane biogenesis.

Inhibition of short-circuit current by triaminopyrimidine in isolated toad urinary bladder

1979 ◽  
Vol 236 (5) ◽  
pp. C221-C224 ◽  
Author(s):  
D. D. Fanestil ◽  
D. A. Vaughn
Keyword(s):  
Urinary Bladder ◽  
High Resistance ◽  
Organic Cation ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Urinary Bladder ◽  
Percent Inhibition ◽  
Irreversible Inhibition ◽  
High Concentrations ◽  
Mucosal Side

The organic cation 2,4,6-triaminopyrimidine (TAP) produced inhibition of short-circuit current (SCC) when added to either the mucosal or serosal surface of the isolated urinary bladder of the toad. Fifty percent inhibition was produced by 10(-3) M TAP in the mucosal solution at pH 6.8 when the mucosal [Na+] was 113 mM. The actions of TAP resemble those produced by amiloride in several ways: a) inhibition of SCC by mucosal application is rapid; b) the mucosal inhibition is fully reversible; c) high concentrations in the serosal solutions produce irreversible inhibition; and d) the concentration required to produce 50% inhibition from the mucosal side is reduced when mucosal [Na+] is reduced. It is postulated that mucosal application of TAP and amiloride inhibit short-circuit current in high-resistance epithelia via action at a common locus.

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