Chloride self exchange in Ehrlich ascites cells. Inhibition by furosemide and 4-acetamido-4′-isothiocyanostilbene-2-2′-disulfonic acid

Aull, Felice; Nachbar, Martin S.; Oppenheim, Joel D.

doi:10.1016/0005-2736(77)90040-2

Cited by 43 publications

(19 citation statements)

References 13 publications

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“…The effects of furosemide upon electrogenic sodium reabsorption were examined in the last series of (27) found that 1 mM furosemide reduced volume reabsorption by 50% in the perfused rat ileum. Similar doses of furosemide (1)(2)(3)(4)(5) mM) also inhibit chloride transport across the erythrocyte membrane (28,29), primarily by inhibiting an anion exchange and transport in many physiological systems (30)(31)(32)(33)(34)(35)(36) …”

Section: Methodsmentioning

confidence: 99%

Effects of Anion-Transport Inhibitors on NaCl Reabsorption in the Rat Superficial Proximal Convoluted Tubule

Lucci¹,

Warnock²

1979

J. Clin. Invest.

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A B S T R A C T The effects of anion-transport inhibitors on volume reabsorption, and total CO2 concentrations were examined by in vivo microperfusion of superficial proximal convoluted tubules of rats. The luminal perfusion solution was a high-chloride, lowbicarbonate solution like that in the in vivo late proximal tubule. The anion-transport inhibitors were only added to the luminal perfusion solutions.In tubules perfused with the control high-chloride solution, the rate of volume reabsorption (J,) was 2.3±0.2 nl/mm min (n = 18), and the collected total CO2 concentration was 4.0±0.3 mM. Furosemide (3 mM) caused a marked reduction in volume reabsorption to 0.8±0.3 nl/mmmin (n = 20) and only a slight increase in the total CO2 concentration of collected samples of perfusate (7.8±0.5 mM). 0.8 mM acetazolamide caused a more pronounced rise in the collected total CO2 concentrations to 10.7±0.5 mM but only a slight fall in J, to 1.7±0.3 nl/mm-min (n = 19). Hence, we inferred that inhibition of carbonic anhydrase only partially accounted for the inhibition of J, by furosemide. 4-acetamido-4'-iso-thiocyanato-stilbene-2,2'-disulphonic acid (0.1 mM), a well-characterized inhibitor of erythrocyte anion exchange mechanisms, also reduced J, to 1.6±0.3 nl/mm min (n = 15) without changing the total CO2 concentrations of the collected perfusates (3.6±0.4 mM). The effect of 4-acetamidoA4'-iso-thiocyanato-stilbene-2,2'-disulphonicPortions of this work were presented at the 10th Annual

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Section: Methodsmentioning

confidence: 99%

Effects of Anion-Transport Inhibitors on NaCl Reabsorption in the Rat Superficial Proximal Convoluted Tubule

Lucci¹,

Warnock²

1979

J. Clin. Invest.

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“…An electrically silent C1-exchange with properties similar to that of the anion exchange system found in red cells and some other cell types (see review by Wieth & Brahm, 1983) has been demonstrated in Ehrlich cells (Levinson & Villereal, 1976;Aull, Nachbar & Oppenheim, 1977;Hoffmann et al, 1979). Moreover, cotransport systems for K+,C1 - (Aull, 1981) or K+,Na+,2C1 - (Geck et al, 1980) have recently been described.…”

Section: Introductionmentioning

confidence: 92%

Na+, Cl− cotransport in Ehrlich ascites tumor cells activated during volume regulation (regulatory volume increase)

1983

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Ehrlich ascites cells were preincubated in hypotonic medium with subsequent restoration of tonicity. After the initial osmotic shrinkage the cells recovered their volume within 5 min with an associated KCl uptake. The volume recovery was inhibited when NO-3 was substituted for Cl-, and when Na+ was replaced by K+, or by choline (at 5 mM external K+). The volume recovery was strongly inhibited by furosemide and bumetanide, but essentially unaffected by DIDS. The net uptake of Cl- was much larger than the value predicted from the conductive Cl- permeability. The undirectional 36Cl flux, which was insensitive to bumetanide under steady-state conditions, was substantially increased during regulatory volume increase, and showed a large bumetanide-sensitive component. During volume recovery the Cl- flux ratio (influx/efflux) for the bumetanide-sensitive component was estimated at 1.85, compatible with a coupled uptake of Na+ and Cl-, or with an uptake via a K+,Na+,2Cl- cotransport system. The latter possibility is unlikely, however, because a net uptake of KCl was found even at low external K+, and because no K+ uptake was found in ouabain-poisoned cells. In the presence of ouabain a bumetanide-sensitive uptake during volume recovery of Na+ and Cl- in nearly equimolar amounts was demonstrated. It is proposed that the primary process during the regulatory volume increase is an activation of an otherwise quiescent, bumetanide-sensitive Na+,Cl- cotransport system with subsequent replacement of Na+ by K+ via the Na+/K+ pump, stimulated by the Na+ influx through the Na+,Cl- cotransport system.

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“…Third, uptake did not approach a maximum as the bath Cl-concentration was raised (Fig. 4), a characteristic of Cl--Cl-exchange processes in many cells (12,17).…”

Section: Resultsmentioning

confidence: 99%

“…Cl-uptake by some cell types includes a component of Cl--Cl-exchange. Often this exchange is inhibited by stilbene sulfonic acids such as 4,4'-diisothiocyanatostilbene-2,2'-sulfonic acid (DIDS) or 4-acetamido-4' isothiocyanotostilbene-2,2'-sulfonic acid (SITS) (12,17). We attempted to determine whether the greater uptake into non-CF cells resulted from the existence of a Cl-exchange mechanism that was missing in CF cells.…”

Section: Resultsmentioning

confidence: 99%

Chloride uptake into cultured airway epithelial cells from cystic fibrosis patients and normal individuals.

Stutts¹,

Cotton²,

Yankaskas³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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The chloride permeability of airway and sweat ductal epithelium of cystic fibrosis (CF) patients is decreased. This abnormality could represent an intrinsic characteristic of the epithelial cell or the response to a tonic extrinsic stimulus, in vivo. We cultured airway epithelial cells derived from CF and non-CF individuals under identical conditions that were free from donor-speciflic factors. Differences in the characteristics of cells that multiplied under these circumstances are unlikely to reflect the effects of extrinsic modulation present in the host. After 8-12 days in culture, the cells of CF and non-CF patients were similar in morphology and intracellular electrolyte content, but the CF cultures took up chloride at a reduced rate. The difference could not be attributed to a higher intracellular potential in CF cells or to the presence of a stilbene anion-sensitive chloride-chloride exchange in non-CF cells. We conclude that epithelial cells from CF patients grown in the absence of extracellular factors of the host express reduced cellular chloride permeability, a defect similar to that found in vivo and in freshly excised nasal epithelium.

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Chloride self exchange in Ehrlich ascites cells. Inhibition by furosemide and 4-acetamido-4′-isothiocyanostilbene-2-2′-disulfonic acid

Cited by 43 publications

References 13 publications

Effects of Anion-Transport Inhibitors on NaCl Reabsorption in the Rat Superficial Proximal Convoluted Tubule

Effects of Anion-Transport Inhibitors on NaCl Reabsorption in the Rat Superficial Proximal Convoluted Tubule

Na+, Cl− cotransport in Ehrlich ascites tumor cells activated during volume regulation (regulatory volume increase)

Chloride uptake into cultured airway epithelial cells from cystic fibrosis patients and normal individuals.

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