Na+ and Cl? transepithelial routes in rabbit gallbladder

Cremaschi, D.; Hénin, S.

doi:10.1007/bf00587337

Cited by 57 publications

(28 citation statements)

References 22 publications

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“…If this value is correct, the total conductance of the basolateral membrane would be too low to permit the exit of C1 in a conductive form even if the entire conductance of this barrier is assigned to the movement of C1. Further, Henin and Cremaschi (1975), Cremaschi and Henin (1975) and van Os and Slegers (1975) have presented evidence suggesting that the baso-lateral membrane is relatively impermeable to C1. These observations await confirmation; however, if they are correct they suggest that C1 exit from the cell, albeit down an electrochemical potential gradient, cannot be due to simple diffusion or a carriermediated facilitated diffusion process that results in the transfer of charge.…”

Section: The Mechanism Of Chloride Exit Across the Baso-laterat Membranementioning

confidence: 95%

Intracellular chloride activities in rabbit gallbladder: Direct evidence for the role of the sodium-gradient in energizing “Uphill” chloride transport

et al. 1978

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Intracellular chloride activities, (Cl)c, in rabbit gallbladder were determined by using conventional (Kcl-filled) microelectrodes and Cl-selective, liquid ion-exchanger, microelectrodes. The results indicated that in the presence of a normal Ringer's solution, (Cl)c averages 35mM; this value is 2.3 times that predicted for an equilibrium distribution across the mucosal and baso-lateral membranes. On the other hand, when the tissue is bathed by Na-free solutions, (Cl)c declines to a value that does not differ significantly from that predicted for an equilibrium distribution. These results, together with those of Frizzell et al. (J. Gen. Physiol. 65:769, 1975) provide, for the first time, compelling evidence that (i) the movement of Cl from the mucosal solution into the cell is directed against an electrochemical potential difference (23mV); and (ii) this movement is energized by coupling to the entry of Na down a steep electrochemical potential difference. Finally, our data suggest that (i) Cl exit from the cell across the basolateral membrane may be coupled to the co-transport of a cation or the countertransport of an anion; and (ii) the mechanism responsible for active Na extrusion from the cell across the baso-lateral membrane is rheogenic (electrogenic), and is not the result of a neutral Na-K exchange.

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Section: The Mechanism Of Chloride Exit Across the Baso-laterat Membranementioning

confidence: 95%

Intracellular chloride activities in rabbit gallbladder: Direct evidence for the role of the sodium-gradient in energizing “Uphill” chloride transport

et al. 1978

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“…Na entry across the mucosal cell membrane was strictly dependent on the presence of Cl-in the mucosal solution and vice versa. This mechanism of neutral coupled NaCl absorption has also been found in rabbit ileum (Nellans, Frizzell & Schultz, 1973) and rabbit gall-bladder (Cremaschi & Henin, 1975). In trout urinary bladder, coupled NaCl co-transport is associated with an undetectable transepithelial potential difference (Vt) and short-circuit current (I,,).…”

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confidence: 64%

Ion‐selective micro‐electrode studies of the electrochemical potentials in trout urinary bladder.

Harvey¹,

Lahlou²

1986

The Journal of Physiology

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SUMMARY1. Intracellular micro-electtode techniques were used to measure the electrical resistances of the cell membranes and the shunt pathway and intracellular ionic activities in trout urinary bladder when the tissue was incubated in Ringer solution and in the presence of the polyene antibiotic ionophore amphotericin B.2. In control conditions the transepithelial potential was zero and the intracellular potential was -56 mV. The intracellular ionic activities measured with singleand double-barrel ion-sensitive micro-electrodes for the first time in a fish bladder (aka = 16 mm, ak = 87 mm, and a'1 = 21 mM) indicate an active accumulation of K and Cl ions and an active extrusion of Na ions by the cell. The maintenance of intracellular Cl activity above its equilibrium value depended on the presence of Na ions in the mucosal medium, but was independent of the presence of K ions.3. Flat cable analysis yielded values for transepithelial, apical, basolateral and shunt resistances of 197, 2790, 1986 and 205 1 cm-2 respectively. Equivalent circuit analysis using amphotericin B yielded similar values for shunt resistance. The paracellular pathway accounts for 96% of transepithelial current flow and this epithelium may be classified as 'leaky'. The cells are electrically coupled with a space constant of 354 sm.4. Amphotericin B when added to the mucosal solution induced an immediate serosa positive transepithelial potential of about 9 mV and a short-circuit current of 64 1zA cm-2. The Vt was ouabain sensitive and dependent on mucosal Na concentration. The origin of the antibiotic induced transepithelial potential was an increase in the sum of the cell membrane electromotive forces. The apical membrane potential depolarized to -7 mV and its resistance fell to 433 Q cm-2. During the first 10 min ofexposure a'a increased to 80 mm and ak decreased to 7 mm with only a small change in ai1. The changes in cellular Na+ and K+ activities were in accordance with their passive redistribution down their electrochemical gradients. 468 B. J. HARVEY AND B. LAHLOU

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“…Thus, it is confirmed that 58 that HCO3-only acts on them. It is noteworthy that, in spite of the fact that HCO3-does not affect the apical conductive Na+ pathways, it significantly diminishes the apical electromotive force because of the decrease in the cell K+ activity it elicits and because of the dominant conductance of this cation at both cell aspects (Henin & Cremaschi, 1975;Cremaschi & Henin, 1975a). Thus, in the rabbit the apical electromotive force (Em), calculated (Cremaschi & Henin 1975a, b;Cremaschi et al 1979).…”

Section: Discussionmentioning

confidence: 99%

“…At the apical membrane it is well documented that both conductive and neutral Na+ pathways exist (Frizzell, Dugas & Schultz, 1975; Henin & Cremaschi, 1975;Cremaschi & Henin, 1975a;Duffey et al 1978;Cremaschi & Meyer, 1982), even though for Necturus gall-bladder Reuss & Finn (1975 b), Reuss & Weinman (1979) and Graf & Giebisch (1979) calculated that the fraction of the transepithelial Na+ flux which could cross the apical barrier through the conductive pathway is only 6-15 00. We have previously demonstrated that Na+ conductance is not affected by HCO3-in the rabbit (Cremaschi & Meyer, 1982) and we can calculate from the data reported here that the net Na+ flux through the apical conductive route is also not modified, in spite of the difference of ENa and Vm in the absence and presence of the anion.…”

Section: Discussionmentioning

confidence: 99%

Bicarbonate effects, electromotive forces and potassium effluxes in rabbit and guinea‐pig gall‐bladder.

Cremaschi¹,

Meyer²,

Rossetti³

1983

The Journal of Physiology

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SUMMARY1. The stimulating effect of external HCO3-on Na+ salt transport has been examined in rabbit and guinea-pig gall-bladder by electrophysiological methods, as a sequel to a previous study carried out by radiochemical techniques.2. At steady state, cell K+ activity was found to be significantly reduced in the presence of HCO3 , whereas cell Na+ activity significantly increased; in parallel the apical membrane p.d. was depolarized; K+ equilibrium potential was higher than membrane p.d. in every case. The apical p.d. dependence on K+ was unaffected by HCO3 , but in the guinea-pig it was affected by Cl-.3. Rapid increases in HCO3-concentration on the luminal side caused a depolarization of the apical p.d. of the guinea-pig within about 30 sec, an effect that did not occur if the tissue was pre-treated with 10-4 M-acetazolamide; the epithelial resistance and apical/basolateral resistance ratio were unchanged in all cases.4. The primary action of HCO3-is confirmed to be on the apical membrane; an HCO3-conductance does not seem to be present at this level, either in the rabbit or guinea-pig, nor does HCO3-affect Na+ influx through the apical conductive pathway, so that all the stimulating effects of the anion are confirmed to be on the neutral transports of Na+ salts; in spite of this, the apical electromotive force is modified due to the changed cell K+ activity. The rapid depolarization caused by the anion in the guinea-pig is in agreement with an HCO3-electrogenic secretion and/or a basolateral conductance for the anion.5. Polyelectrolyte dissociation from protons increases in the absence of external HCO3-: the negative charges are mainly counterbalanced by bound Na+ in the rabbit and by free K+ in the guinea-pig.6. K+ leakage from the cell into the lumen is calculated to be minimal in the rabbit and all K+ lost could be reabsorbed through the paracellular pathways; K+ efflux to the subepithelial layer via conductive routes is insufficient to account for the over-all K+ efflux.

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Na+ and Cl? transepithelial routes in rabbit gallbladder

Cited by 57 publications

References 22 publications

Intracellular chloride activities in rabbit gallbladder: Direct evidence for the role of the sodium-gradient in energizing “Uphill” chloride transport

Intracellular chloride activities in rabbit gallbladder: Direct evidence for the role of the sodium-gradient in energizing “Uphill” chloride transport

Ion‐selective micro‐electrode studies of the electrochemical potentials in trout urinary bladder.

Bicarbonate effects, electromotive forces and potassium effluxes in rabbit and guinea‐pig gall‐bladder.

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