Time course of active Na transport and oxidative metabolism following transepithelial potential perturbation in toad urinary bladder

1981 ◽  
Vol 63 (3) ◽  
pp. 157-163 ◽  
Author(s):  
Stanley J. Rosenthal ◽  
John G. King ◽  
Alvin Essig
Keyword(s):  
Urinary Bladder ◽  
Oxidative Metabolism ◽  
Time Course ◽  
Toad Urinary Bladder ◽  
Na Transport ◽  
Transepithelial Potential ◽  
Potential Perturbation

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.

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.

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.

scholarly journals Ca(2+)-blockable, poorly selective cation channels in the apical membrane of amphibian epithelia. Tetracaine blocks the UO2(2+)-insensitive pathway.

1993 ◽  
Vol 101 (1) ◽  
pp. 103-116 ◽  
Author(s):  
L Desmedt ◽  
J Simaels ◽  
W Van Driessche
Keyword(s):  
Urinary Bladder ◽  
Time Course ◽  
Rana Temporaria ◽  
Noise Analysis ◽  
Inhibitory Effect ◽  
The Other ◽  
Cation Channels ◽  
Toad Urinary Bladder ◽  
Amphibian Epithelia ◽  
Microelectrode Measurements

We examined the effect of the local anesthetic tetracaine on the Ca(2+)-blockable, poorly selective cation channels in the isolated skin of Rana temporaria and the urinary bladder of Bufo marinus using noise analysis and microelectrode impalements. Experiments with frog skin demonstrated that mucosal concentrations of the compound up to 100 microM did not affect the Na+ current through type S channels (slowly fluctuating, UO2(2+)-blockable channels) and the associated noise. On the other hand, 20 microM mucosal tetracaine already suffices to inhibit approximately 50% of the current carried by Cs+ and Na+ through channel type F (fast fluctuating, UO2(2+)-insensitive channel) and So of the associated Lorentzian component. With 100 microM of the inhibitor the current and So values were reduced by at least 70-80%. The time course of the response to serosal tetracaine was markedly slower and the effects on the current and So were smaller. Possible effects on the basolateral K+ conductance were excluded on the basis of the lack of response of transepithelial K+ movements to 100 microM tetracaine. UO2(2+) and tetracaine together blocked the poorly selective cation pathways almost completely. Moreover, both agents retain their inhibitory effect in the presence of the other. In toad urinary bladder, the Ca(2+)-blockable channel is also tetracaine blockable. The concentration required for half-maximal inhibition is approximately 100 microM in SO4(2-) and approximately 20 microM in Cl-. The data with tetracaine complement those obtained with UO2(2+) and support the idea that the Ca(2+)-blockable current proceeds through two distinct classes of cation channels. Using tetracaine and UO2(2+) as channel-specific compounds, we demonstrated with microelectrode measurements that both channel types are located in the granulosum cells.

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.

Calcitonin is a competitive inhibitor of the hydrosmotic effect of oxytocin in toad bladder

1988 ◽  
Vol 255 (5) ◽  
pp. E613-E616
Author(s):  
M. Parisi ◽  
C. Ibarra ◽  
M. Ladizesky ◽  
C. Mautalen
Keyword(s):  
Urinary Bladder ◽  
Time Course ◽  
Water Flux ◽  
Competitive Inhibitor ◽  
Intracellular Camp ◽  
Toad Urinary Bladder ◽  
The One ◽  
Toad Bufo ◽  
Camp Levels ◽  
Dose Dependent

The effects of calcitonin (CT) on the water transfer in the toad (Bufo arenarum) urinary bladder, an epithelial barrier commonly employed as a model of the mammalian nephron, were studied. The net transmembrane water flux was measured at minute intervals, while the endogenous adenosine 3',5'-cyclic monophosphate (cAMP) levels were determined in isolated epithelial cells. It was observed that 1) CT, up to 10(-6) M, did not have any effect on water permeability. 2) Preincubation with CT, between 10(-7) and 10(-8) M, inhibited the hydrosmotic response to a supramaximal dose of oxytocin (OXT; 2 x 10(-8) M), used here as an antidiuretic hormone (ADH) analogue. This inhibition was reversible and concentration related. Nevertheless, although the magnitude of the response was reduced, its time course of evolution did not change. 3) When CT was added on the previously developed response to OXT, inhibition was also dose dependent with a time course not distinguishable from hormonal washout. 4) CT, up to 10(-6) M, did not modify the hydrosmotic response to 8-bromo cAMP, a potent analogue of the ADH second messenger. 5) CT and OXT increased the intracellular cAMP levels, but both effects were not cumulative. The increase induced by CT plus OXT was significantly lower than the one elicited by OXT alone. It is concluded that CT is a competitive inhibitor to the hydrosmotic effect of OXT in toad urinary bladder. Its action must be located prior to cAMP formation.

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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