Interaction of heptanol and pressure on sodium and chloride transport by toad skin

1990 ◽  
Vol 69 (5) ◽  
pp. 1883-1892 ◽  
Author(s):  
M. Li ◽  
S. K. Hong ◽  
J. M. Goldinger ◽  
M. E. Duffey
Keyword(s):  
Channel Blocker ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Na Transport ◽  
Toad Skin ◽  
Shunt Resistance ◽  
Cl Conductance

We examined the interaction of heptanol and hydrostatic pressure on Na+ and Cl- transport in isolated toad skin. In the presence of Cl-, heptanol decreased short-circuit current (Isc) and total transepithelial resistance (Rt). However, in the absence of Cl- in the mucosal bath, heptanol increased Rt, although it retained the same inhibitory effect on Isc. When transepithelial active Na+ transport was blocked by amiloride, heptanol had no effect on Isc whether or not Cl- was present, whereas it decreased the shunt resistance (Rs) only in the presence of Cl- in the mucosal bath. Moreover, this effect of heptanol on Rs was significantly smaller in the presence of diphenylamine-2-carboxylate (DPC), a known Cl- channel blocker. Pressure also decreased Isc through inhibition of active Na+ transport, but it increased Rs. When heptanol and pressure were applied together, their inhibitory effects on Isc were additive, but their effects on Rs were antagonistic. Furthermore, when a transepithelial Cl- current was produced by reducing the Cl- concentration of the serosal bath, heptanol stimulated this current, which was reversibly inhibited by pressure or DPC addition to the mucosal bath. When the heptanol-stimulated Cl- current was first inhibited by pressure, subsequent DPC addition had less or no effect. These results suggest that one site of an antagonistic interaction of heptanol and pressure in toad skin is an apical membrane Cl- conductance.

Na+ transport in normal and CF human bronchial epithelial cells is inhibited by BAY 39-9437

2001 ◽  
Vol 281 (1) ◽  
pp. L16-L23 ◽  
Author(s):  
Robert J. Bridges ◽  
Ben B. Newton ◽  
Joseph M. Pilewski ◽  
Daniel C. Devor ◽  
Christopher T. Poll ◽  
...  
Keyword(s):  
Serine Protease ◽  
Half Life ◽  
Inhibitory Concentration ◽  
Therapeutic Potential ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Human Bronchial Epithelial Cells ◽  
Na Transport ◽  
Bronchial Epithelial

To test the hypothesis that Na+ transport in human bronchial epithelial (HBE) cells is regulated by a protease-mediated mechanism, we investigated the effects of BAY 39-9437, a recombinant Kunitz-type serine protease inhibitor, on amiloride-sensitive short-circuit current of normal [non-cystic fibrosis (CF) cells] and CF HBE cells. Mucosal treatment of non-CF and CF HBE cells with BAY 39-9437 decreased the short-circuit current, with a half-life of ∼45 min. At 90 min, BAY 39-9437 (470 nM) reduced Na+ transport by ∼70%. The inhibitory effect of BAY 39-9437 was concentration dependent, with a half-maximal inhibitory concentration of ∼25 nM. Na+ transport was restored to control levels, with a half-life of ∼15 min, on washout of BAY 39-9437. In addition, trypsin (1 μM) rapidly reversed the inhibitory effect of BAY 39-9437. These data indicate that Na+transport in HBE cells is activated by a BAY 39-9437-inhibitable, endogenously expressed serine protease. BAY 39-9437 inhibition of this serine protease maybe of therapeutic potential for the treatment of Na+ hyperabsorption in CF.

Selective effects of bumetanide on chloride transport in bullfrog cornea

1978 ◽  
Vol 234 (4) ◽  
pp. F297-F301
Author(s):  
O. A. Candia ◽  
H. F. Schoen
Keyword(s):  
Electrical Resistance ◽  
Loop Diuretic ◽  
Chloride Transport ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Selective Inhibitor ◽  
O2 Consumption ◽  
Na Transport ◽  
Bathing Medium

Frog corneas were mounted in a modified Ussing chamber and short-circuit current (SCC) and unidirectional Cl fluxes were measured. Bumetanide, a loop diuretic, at concentrations as low as 10(-7) M, reduced the SCC 29%. At 10(-5) M, bumetanide reduced the SCC 96% and increased transcorneal electrical resistance 20-51%. The forward Cl flux declined from 0.71 +/- 0.04 to 0.20 +/- 0.03 mueq/h.cm2 (n, 7), while, in separate experiments, the backward Cl flux did not change significantly (from 0.22 +/- 0.03 to 0.23 +/- 0.04; n, 7). When corneas were mounted in Cl-free Ringer and the net Na transport was stimulated with amphotericin B, 10(-5) M bumetanide had no effect on the SCC. In separate experiments the effect of 10(-5) M bumetanide on the O2 consumption was measured in a stirrer bath assembly. Bumetanide decreased the O2 consumption from 352 +/- 14 to 297 +/- 19 microliter/h.cm2 (significantly different from sham-treated controls). This decrease was similar to that obtained with furosemide or when Cl was removed from the bathing medium. We infer from these results that bumetanide is a selective inhibitor of active Cl transport in the bullfrog cornea.

Ba2+ inhibition of electrogenic Cl- secretion in vitro frog and piglet gastric mucosa

1980 ◽  
Vol 239 (3) ◽  
pp. G151-G160 ◽  
Author(s):  
W. L. McLennan ◽  
T. E. Machen ◽  
T. Zeuthen
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Surface Charges ◽  
Inhibitory Effects ◽  
Cl Secretion ◽  
High K ◽  
In Vitro Investigation ◽  
Newborn Pigs

Gastric mucosae from frogs and newborn pigs were used for in vitro investigation of the effects of Ba2+ (10 microM to 7 mM) on transepithelial potential difference (PD), resistance and conductance (G), short-circuit current (Isc), H+ secretion, and transepithelial fluxes of 36Cl-. Ba2+ in the serosal, but not the mucosal, solution of both preparations caused PD, G, Isc, and Cl- secretion (JnetCl, Isc conditions) to decrease, while H+ secretion remained constant. Because the oxyntic cells were most likely the site of action for Ba2+, these cells must have the capacity to secrete Cl- in excess of H+ ions. The inhibitory effect of Ba2+ was not due to competition in the serosal membrane by Ba2+ for surface charges, Ca2+ sites, Na+ sites, or Cl- sites. When [K+] in both the mucosal and serosal solutions or in just the serosal solution ([K+]s) alone was increased to 10 mM, the inhibitory effects of low [Ba2+] were reduced; however, at higher [Ba2+], Isc was stimulated. At least part of the Ba2+ effect seems to be due to blockage of K+ channels in the serosal membrane of oxyntic cells. High [K+]s also caused decreased PD and Isc (but increased G) with no change in H+ secretion. It is proposed that during Isc conditions, JnetCl involves a neutral Na+-dependent accumulation of Cl- within oxyntic cells and a passive, conductive efflux fromthe cells into the mucosal solution. Ba2+ and high [K+] may alter this transport by depolarizing and, under certain conditions, hyperpolarizing intracellular voltage.

scholarly journals THE INHIBITORY EFFECT OF STROPHANTHIDIN ON SECRETION BY THE ISOLATED GASTRIC MUCOSA

1959 ◽  
Vol 42 (6) ◽  
pp. 1233-1239 ◽  
Author(s):  
I. L. Cooperstein
Keyword(s):  
Gastric Mucosa ◽  
Chloride Transport ◽  
Short Circuit ◽  
Membrane Conductance ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Transport Systems ◽  
Anion Secretion ◽  
Diffusion Component ◽  
Sodium And Potassium

The unidirectional fluxes of Na+ and Cl- were measured across the isolated gastric mucosa of the bullfrog (R. catesbiana). The addition of strophanthidin, a cardiac aglycone, resulted in marked reductions of the spontaneous potential and short-circuit current. Associated with these changes, the isolated gastric mucosa ceased secreting chloride and hydrogen ion. Although the active component of chloride transfer was inhibited, the exchange diffusion component seemed to increase. No significant changes in membrane conductance or sodium flux were noted. Possible mechanisms of strophanthidin inhibition were discussed in view of its effect on chloride transport across the gastric mucosa and on sodium and potassium transfer in other tissues. It was concluded that the cardiac glycosides may not be specific inhibitors of sodium and potassium transport. This non-specific inhibition suggests that active chloride transport is affected by strophanthidin directly and/or anion secretion is dependent upon normal functioning of cation transport systems in the tissue.

Failure of 16,16-dimethyl PGE2 to prevent inhibitory effect of ethanol on sodium transport in canine gastric mucosa

1985 ◽  
Vol 248 (3) ◽  
pp. G299-G306
Author(s):  
T. A. Miller ◽  
J. M. Henagan ◽  
Y. J. Kuo ◽  
L. L. Shanbour
Keyword(s):  
Gastric Mucosa ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Gastric Epithelium ◽  
Bathing Solution ◽  
Inhibitory Effects ◽  
Stimulation Of

By use of an in vitro canine gastric mucosal preparation, we evaluated the effects of ethanol (2, 4, 6, and 8%, vol/vol) and indomethacin (2.2 X 10(-4)M), with and without 16,16-dimethyl PGE2 pretreatment, on net sodium transport (JNanet) (mucosal to serosal) across gastric epithelium. Although administration of 2 or 4% ethanol to the mucosal bathing solution had no appreciable inhibitory effects on sodium transport, 6 and 8% ethanol and indomethacin significantly inhibited JNanet when compared with untreated control mucosa. This effect was accompanied by inhibition of transmucosal potential difference (PD) and short-circuit current (Isc). In other mucosae exposed to dimethyl PGE2 (8 X 10(-6) M) in the serosal bathing solution, significant increases in JNanet, PD, and Isc were noted when compared with control mucosa. Addition of 6 or 8% ethanol to the mucosal solution of dimethyl PGE2-pretreated tissue resulted in significant decreases in PD, Isc, and JNanet below control values that were not significantly different from mucosa exposed to 6 and 8% ethanol without PG pretreatment. When indomethacin was added to the mucosal solution following dimethyl PGE2 pretreatment, only slight decreases in PD and Isc below control levels were observed, and the inhibitory effects on JNanet induced by indomethacin without such treatment were abolished. These findings suggest that stimulation of JNanet by prostaglandin may play a role in its ability to prevent indomethacin damage to gastric epithelium but does not appear to be of importance in mediating protection against ethanol damage.

Inhibitory effect of phorbol ester on sodium transport in frog urinary bladder

1990 ◽  
Vol 259 (3) ◽  
pp. F425-F431
Author(s):  
T. Satoh ◽  
H. Endou
Keyword(s):  
Urinary Bladder ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Inhibitory Influence ◽  
Dependent Manner ◽  
Camp Accumulation ◽  
Frog Urinary Bladder ◽  
Na Transport

To confirm the role of protein kinase C (PKC) on epithelial Na transport, we studied the effects of phorbol 12-myristate 13-acetate (PMA) and dioctanoylglycerol (DiC8), activators of PKC, on short-circuit current (Isc) in frog urinary bladder and further examined the influence of sphingosine, an inhibitor of PKC, on PMA- or DiC8-modulated Isc. PMA reduced basal Isc in a dose-dependent manner, and sphingosine (10 and 100 microM) partially restored PMA-reduced Isc. On the other hand, DiC8 (5 x 10(-5) M) also reduced basal Isc, and this action was completely prevented by 100 microM sphingosine. Both PMA (4 x 10(-5) M) and DiC8 inhibited vasopressin (50 mU/ml)- and forskolin (5 x 10(-5) M)-stimulated increases in Isc. PMA (4 x 10(-5) M) also inhibited 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP)-stimulated increase in Isc. Furthermore, PMA (4 x 10(-5) M) and DiC8 (5 x 10(-5) M) inhibited vasopressin (50 mU/ml)-stimulated cAMP accumulation. DiC8 also inhibited forskolin-stimulated cAMP accumulation. These results indicate that PMA exerts inhibitory influence on Na transport mainly by its own potency of PKC activation. In addition, it is suggested that there is a cross talk in epithelial Na transport between PKC and cAMP-dependent pathway in frog urinary bladder.

Interaction between sodium and chloride transport in canine tracheal mucosa

1979 ◽  
Vol 46 (1) ◽  
pp. 111-119 ◽  
Author(s):  
F. J. Al-Bazzaz ◽  
Q. Al-Awqati
Keyword(s):  
Hormonal Regulation ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Na Transport ◽  
Tracheal Mucosa ◽  
Electrically Conductive ◽  
Ussing Chambers ◽  
Cl Secretion ◽  
Cl Transport

Canine tracheal mucosae were dissected and mounted as flat sheets in Ussing chambers. Unidirectional isotope fluxes of 22Na and 36Cl were performed across paired mucosae from the same animal. The average spontaneous potential difference was 42 + 1.2 mV (mean +/- SE) lumen negative. The short-circuit current (SCC) 3.09 +/- 0.36 mueq/cm2.h was accounted for by a net Cl secretion of 2.46 +/- 0.26 mueq/cm2.h toward the mucosa and net Na absorption of 0.46 +/- 0.13 mueq/cm2.h toward submucosa. Removal of Cl depressed SCC but had no effect on unidirectional or net Na transport (n = 7). By contrast, removal of Na (n = 6) or the addition of ouabain (n = 7) abolished net Cl secretion and greatly reduced SCC. Theophylline (n = 6) added to the submucosal bath no significant effect on Na transport but stimulated SCC and Cl secretion, suggesting hormonal regulation of Cl transport. The results suggest that the active transport of Na and Cl in this epithelium occur by electrically conductive pathways, i.e., the transport is “electrogenic.” Further it appears that Na transport is independent of the presence of Cl but that Cl transport depends on some parameter of active Na transport.

Chloride transport inhibition by piretanide and MK-196 in bullfrog corneal epithelium

1981 ◽  
Vol 240 (1) ◽  
pp. F25-F29
Author(s):  
O. A. Candia ◽  
H. F. Schoen ◽  
L. Low ◽  
S. M. Podos
Keyword(s):  
Corneal Epithelium ◽  
Electrical Resistance ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Na Transport ◽  
Cl Transport ◽  
Apical Side ◽  
Diuretic Agents ◽  
Cl Permeability

Two new diuretic agents, piretanide and MK-196, inhibited short-circuit current (SCC) across the isolated frog corneal epithelium. The effect is explained as an inhibition of active Cl transport. A definite decrease in SCC and an increase in electrical resistance was observed with both diuretics in concentrations as low as 10(-6) M. Piretanide, at 10(-4) M, reduced the SCC by 90%, reduced th unidirectional forward Cl flux from 0.60 to 0.28 mueq x h-1 x cm-2, and increased the resistance by 60%. There was no effect on the Cl backflux. At 10(-4) M, MK-196 reduced the SCC by 83% and increased the resistance by 72%, from 1.68 to 2.91 k omega x cm2. Replacement of Cl by SO4 in the bathing solutions resulted in a larger increase in resistance, from 1.68 to 3.80 k omega x cm2. The diuretics had no effect on active Na transport across the corneal epithelium. After the permeability of the apical side was increased by amphotericin B, the drugs could not inhibit the Cl-originated SCC. These results suggest that piretanide and MK-196 selectively inhibit active Cl transport in the cornea by blocking Cl permeability of the apical side of the epithelial cells.

Thyroxine and Na+ transport in toad: role in transition from poikilo- to homeothermy

1979 ◽  
Vol 236 (3) ◽  
pp. C117-C124 ◽  
Author(s):  
B. C. Rossier ◽  
M. Rossier ◽  
C. S. Lo
Keyword(s):  
Urinary Bladder ◽  
Atpase Activity ◽  
Short Circuit ◽  
Stage Iv ◽  
Short Circuit Current ◽  
Inhibitory Effect ◽  
Base Line ◽  
Na Transport ◽  
Tissue Resistance

The effects of thyroxine (T4) on Na+ transport, oxygen consumption (QO2), and Na+-K+-ATPase activity were studied in the urinary bladder and liver of the toad Bufo marinus. In the bladder, T4 in vitro (10(-8) to 10(-6) M) had no significant effect on these parameters during 15 h of incubation. When injected intraperitoneally (approximately 20 microgram/(kg body wt.day) for 6 days), T4 lowered base-line, short-circuit current by 62% (P less than 0.0025) and potential difference by 37% (P less than 0.001), increasing tissue resistance by 40% (P less than 0.02). T4 depressed QO2/DNA (-25%, P less than 0.05) with no significant effect on Na+-K+-ATPase activity. In liver, T4 increased the recovery per cell DNA of mitochondrial proteins by 32% (P less than 0.025), corresponding to an increased QO2 (stage IV) of isolated mitochondria per cell DNA (+54%, P less than 0.01). There was no significant effect on Na+-K+-ATPase activity. These results suggest that, unlike its function in the rat, T4 in the toad does not regulate cellular thermogenesis by inducing Na+-K+-ATPase. This major difference could account at least in part for the transition from poikilothermy to homeothermy. In addition, T4 has a distinct inhibitory effect on Na+ transport in the urinary bladder, which suggests an antagonism to the action of aldosterone.

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