Transport by isolated rabbit gallbladders in phosphate-buffered solutions

Sullivan, B.; Berndt, William O.

doi:10.1152/ajplegacy.1973.225.4.838

Cited by 15 publications

(7 citation statements)

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“…Inhibition of gall-bladder net fluid transport by ETCA does not either seem to be mediated by inhibition of oxidative metabolism, since mucosal application of 10-3 M-ETCA caused a 85% inhibition of net fluid transport rate by inhibitors of oxidative metabolism like N2 or 2,4-DNP was accompanied by a marked depression of p.d., in agreement with previous observations (Sullivan & Berndt, 1973).…”

Section: Effectssupporting

confidence: 94%

“…Fig. 2) in order to abolish gall-bladder net fluid transport is in agreement with previous observations (Diamond, 1962;Dietschy, 1964;Martin & Diamond, 1966;Sullivan & Berndt, 1973) and with the localization of the ouabain sensitive ATPase (Skou, 1965) (Kaye, Wheeler, Whitlock & Lane, 1966). The full dose-response curve shown in Fig.…”

Section: Gall-bladder Transport Mechanismssupporting

confidence: 92%

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Functional distinction between two transport mechanisms in rabbit gall‐bladder epithelium by use of ouabain, ethacrynic acid and metabolic inhibitors.

Frederiksen¹

1978

The Journal of Physiology

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SUMMARY1. Net fluid transport rate, transepithelial p.d. and resistance, and unidirectional Na+-fluxes were measured in rabbit gall-bladder preparations exposed on both sides to bicarbonate-Ringer solution in vitro.2. Both ouabain and ethacrynic acid (ETCA) caused dose-dependent decreases of net fluid transport rate; ouabain inhibited fluid transport predominantly from the serosal side, whereas the inhibitory effect of ETCA was elicited mainly from the mucosal (luminal) side. Applied bilaterally, the ID50 for ouabain was 2-5 x 10-6 M, and for ETCA 2-3 x 104 M. After maximal inhibition at each concentration level of the two inhibitors fluid transport could not be reversed.3. 2,4-Dinitrophenol (2,4-DNP) (2 x 104 M) or substitution of 02 by N2 caused an 80% reversible decrease of net fluid transport.4. The spontaneous p.d. across the rabbit gall-bladder was about 2-7 mV, mucosal side positive. 2,4-DNP, N2 and serosal application of ouabain depressed the p.d. after an initial hyperpolarization. This decrease was reversible during recovery from 2,4-DNP and N2, but irreversible after removal of ouabain at concentrations > 10-4 M. Mucosal application of ETCA (10-3 M) caused no decrease in p.d., which actually increased slightly.5. Calculated passive serosal-to-mucosal Na+-fluxes changed in the same direction as did changes in conductance.6. It is concluded that ETCA does not interfere primarily with the Na-K-ATPase or cellular oxidative metabolism. The data support the proposal that the pump responsible for isosmotic transepithelial fluid transfer is located in the luminal end of the cells. This pump is ETCA-sensitive. The ATPase-dependent Na-K pump, which can be inhibited by ouabain, is localized in the serosa-facing cell membrane. The data suggest that the inhibition of net fluid transport by ouabain is indirect and mediated by changes in intracellular ion concentrations.7. The results support the concept that the transepithelial fluid transport mechanism is electroneutral, and suggest that the mucosa positive transepithelial p.d. is due to differences in electromotive forces arising from ion (mainly K+) diffusion across the mucosal and serosal cell membranes. FREDERIKSEN

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Section: Effectssupporting

confidence: 94%

Section: Gall-bladder Transport Mechanismssupporting

confidence: 92%

Functional distinction between two transport mechanisms in rabbit gall‐bladder epithelium by use of ouabain, ethacrynic acid and metabolic inhibitors.

Frederiksen¹

1978

The Journal of Physiology

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“…Chloride entry into the cell is Na + dependent and inhibitable by SCN- Cremaschi et al, 1979), 1 an anion which competes for carrier-mediated CItransport in many epithelial cells (Katz et al, 1982). In this paper we showed that SCN-action is immediate and that the 25-ram concentration used in the past on this tissue (Sullivan & Berndt, 1973;Van Os, Michels & Slegers, 1976;Cremaschi et al, 1979) gives rapid maximal effects.…”

Section: The Nature Of the Cotransport In Rabbit Gallbladdermentioning

confidence: 72%

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: I. Na+/H+, Cl−/HCO 3 − double exchange and Na+−Cl− symport

et al. 1987

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“…The decrease in bilary bicarbonate concentration would seem to be due to the dilution of a bicarbonate-containing fluid with a solution of sodium chloride. Sullivan & Berndt (1973a, b) have studied the reabsorptive properties of the isolated rabbit gall-bladder, and have found that acetazolamide and 2,4-DNP depress volume transport in this organ. In the present work, salicylate, which resembles 2,4-DNP in its action on the biliary system, and acetazolamide have been shown to act as choleretics.…”

Section: Other Experimentsmentioning

confidence: 99%

The effect of sodium salicylate on bile secretion in the dog.

Rutishauser¹,

Stone²

1975

The Journal of Physiology

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SUMMARY1. The i.v. injection of sodium salicylate (100 mg/kg) in the dog caused a rapid and maintained choleresis of the order of 300-600% of control levels.2. The total amount of salicylate excreted in bile was only 1-2 % of that injected.3. The secretion of bile salt into bile was not increased by salicylate. 4. The choleresis caused by salicylate was associated with a decrease in the concentrations of sodium and of bile salt in bile, and with an increase in the concentration of chloride; the biliary concentration of bicarbonate was either temporarily increased or unchanged.5. The choleresis could not be inhibited by the intra-portal injection of ouabain (0.1 mg/kg).6. The secretion of bromsulphthalein into bile was not potentiated by the choleresis.7. The choleretic efficiency of sodium taurocholate was not increased in the presence of salicylate.8. The injection of acetazolamide (20 mg/kg), in the presence of a salicylate choleresis, caused an increase in the osmolality of bile and an increase in biliary sodium concentration, such that the composition of bile more nearly approached that of plasma.9. The possible mechanisms underlying the choleretic effect of sodium salicylate are discussed.

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Transport by isolated rabbit gallbladders in phosphate-buffered solutions

Cited by 15 publications

References 0 publications

Functional distinction between two transport mechanisms in rabbit gall‐bladder epithelium by use of ouabain, ethacrynic acid and metabolic inhibitors.

Functional distinction between two transport mechanisms in rabbit gall‐bladder epithelium by use of ouabain, ethacrynic acid and metabolic inhibitors.

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: I. Na+/H+, Cl−/HCO 3 − double exchange and Na+−Cl− symport

The effect of sodium salicylate on bile secretion in the dog.

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