Cell Cl and transepithelial Na transport in toad urinary bladder

1994 ◽  
Vol 142 (1) ◽  
Author(s):  
A.G. Butt ◽  
C.W. McLaughlin ◽  
J.M. Bowler ◽  
R.D. Purves ◽  
A.D.C. Macknight
Keyword(s):  
Urinary Bladder ◽  
Toad Urinary Bladder ◽  
Na Transport ◽  
Transepithelial Na Transport

Effects of anions on cellular volume and transepithelial Na+ transport across toad urinary bladder

1985 ◽  
Vol 83 (1-2) ◽  
pp. 119-137 ◽  
Author(s):  
Simon A. Lewis ◽  
A. Grant Butt ◽  
M. Joanne Bowler ◽  
John P. Leader ◽  
Anthony D. C. Macknight
Keyword(s):  
Urinary Bladder ◽  
Toad Urinary Bladder ◽  
Na Transport ◽  
Cellular Volume ◽  
Transepithelial Na Transport

Use of mass spectrometer to measure CO2 and O2 fluxes in voltage-clamped epithelia

1979 ◽  
Vol 236 (4) ◽  
pp. F413-F418
Author(s):  
S. J. Rosenthal ◽  
J. G. King ◽  
A. Essig
Keyword(s):  
Urinary Bladder ◽  
Mass Spectrometer ◽  
Ussing Chamber ◽  
Electrical Current ◽  
Toad Urinary Bladder ◽  
Co2 Efflux ◽  
Quadrupole Mass ◽  
Active Sodium ◽  
Na Transport ◽  
Made In

A quadrupole mass spectrometer was coupled to an Ussing chamber in order to evaluate rates of oxidative metabolism in voltage-clamped epithelia. Well-defined mixing characteristics of the continuously perfused chamber allowed CO2 and O2 concentrations to be related to rates of CO2 efflux, JCO2, and oxygen influx, JO2. The use of a model tissue to simulate step changes in JCO2 validated the treatment, with response within a minute. Monitoring of metabolism was facilitated by use of a desk-top computer, which evaluated JCO2 at 6-s intervals. Concurrent measurements of electrical current and JCO2 were made in the toad urinary bladder in order to relate active sodium transport to metabolism; the use of amiloride to eliminate active transport and the associated metabolism then allowed evaluation of the rates of active Na transport (JNa) and suprabasal metabolism (JsbCO2), and their ratio JNa/JsbCO2. We report the ability to resolve a 5 pmol/s change in CO2 efflux or an 11 pmol/s change in O2 influx rates.

Effects of tetracyclines on aldosterone- and insulin-mediated Na+ transport in the toad urinary bladder

1979 ◽  
Vol 552 (1) ◽  
pp. 162-168 ◽  
Author(s):  
Malcolm Cox ◽  
Joseph Guzzo ◽  
Allan Shook ◽  
Gary Huber ◽  
Irwin Singer
Keyword(s):  
Urinary Bladder ◽  
Toad Urinary Bladder ◽  
Na Transport

Insulin-like growth factor 1 stimulates renal epithelial Na+ transport

1988 ◽  
Vol 255 (3) ◽  
pp. C413-C417 ◽  
Author(s):  
B. L. Blazer-Yost ◽  
M. Cox
Keyword(s):  
Protein Synthesis ◽  
Growth Factor ◽  
Urinary Bladder ◽  
Classical Model ◽  
Na Channel ◽  
Toad Urinary Bladder ◽  
Insulin Like Growth Factor ◽  
Distal Nephron ◽  
Na Transport ◽  
New Protein

Insulin-like growth factor 1 (IGF1) stimulates vectorial Na+ transport in a classical model of the mammalian distal nephron, the toad urinary bladder. Net mucosal to serosal Na+ flux is stimulated by concentrations of IGF1 as low as 0.1 nM, and the response is maximal at 10 nM. Na+ transport increases within minutes of the serosal addition of IGF1, reaches a maximum in 2-3 h, and is sustained for at least 5 h. Neither the initial nor the sustained response to IGF1 is dependent on a new protein synthesis. The IGF1 response is inhibited by a concentration of amiloride (10(-5) M) that is known to specifically block the conductive apical Na+ channel but that has little effect on the Na+-H+ antiporter. Further studies will be necessary to establish a role for this growth factor in normal renal epithelial function, but it is possible that the natriferic and growth-stimulatory effects of IGF1 are intimately related.

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.

scholarly journals Sodium transport effects on the basolateral membrane in toad urinary bladder.

1982 ◽  
Vol 80 (5) ◽  
pp. 733-751 ◽  
Author(s):  
C W Davis ◽  
A L Finn
Keyword(s):  
Urinary Bladder ◽  
Time Course ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Membrane Resistance ◽  
Membrane Voltage ◽  
Toad Urinary Bladder ◽  
Na Transport ◽  
Bladder Epithelium ◽  
Current Output

In toad urinary bladder epithelium, inhibition of Na transport with amiloride causes a decrease in the apical (Vmc) and basolateral (Vcs) membrane potentials. In addition to increasing apical membrane resistance (Ra), amiloride also causes an increase in basolateral membrane resistance (Rb), with a time course such that Ra/Rb does not change for 1-2 min. At longer times after amiloride (3-4 min), Ra/Rb rises from its control values to its amiloride steady state values through a secondary decrease in Rb. Analysis of an equivalent electrical circuit of the epithelium shows that the depolarization of Vcs is due to a decrease in basolateral electromotive force (Vb). To see of the changes in Vcs and Rb are correlated with a decrease in Na transport, external current (Ie) was used to clamp Vmc to zero, and the effects of amiloride on the portion of Ie that takes the transcellular pathway were determined. In these studies, Vcs also depolarized, which suggests that the decrease in Vb was due to a decrease in the current output of a rheogenic Na pump. Thus, the basolateral membrane does not behave like an ohmic resistor. In contrast, when transport is inhibited during basolateral membrane voltage clamping, the apical membrane voltage changes are those predicted for a simple, passive (i.e., ohmic) element.

Insulin-mediated Na+ transport in the toad urinary bladder

1977 ◽  
Vol 232 (3) ◽  
pp. F270-F277
Author(s):  
M. Cox ◽  
I. Singer
Keyword(s):  
Urinary Bladder ◽  
Initial Rate ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Mechanisms Of Action ◽  
Maximal Response ◽  
Toad Urinary Bladder ◽  
Na Transport ◽  
Ussing Chambers ◽  
K Concentration

The characteristics of insulin-induced Na+ transport in the toad urinary bladder were determined and compared to those of aldosterone. Bladders were mounted in modified Ussing chambers, and standard short-circuit current techniques were employed to measure transepithelial Na+ transport. Insulin added to the serosal medium is much more effective than insulin added to the mucosal medium. Serosal insulin concentrations from 10(1) to 10(3) muU/ml increase both the initial rate and the final level of Na+ transport achieved, whereas concentrations from 10(3) to 10(5) muU/ml increase only the initial rate of Na+ transport. Insulin-induced Na+ transport probably does not require glucose. Both insulin- and aldosterone-induced Na+ transport are directly proportional to serosal (but not mucosal) K+ concentration over the physiologic range (2.0-7.0 meq/liter). However, cycloheximide abolishes aldosterone- but not insulin-induced Na+ transport. In addition, insulin stimulates Na+ transport after a maximal response to aldosterone, and aldosterone stimulates Na+ transport after a maximal response to insulin. Thus, although they have several similar characteristics, insulin and aldosterone have at least partially independent mechanisms of action on Na+ transport in the toad urinary bladder.

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