Influence of loop diuretics and anions on passive potassium influx into human red cells.

Chipperfield, A. R.

doi:10.1113/jphysiol.1985.sp015888

Cited by 13 publications

(8 citation statements)

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“…These are mediated by the Na+/ Na + (Na+/Li +) exchange system [13] and by the so-called Na+-K + cotransport system [44] which is dependent on chloride [7,21] and blocked by loop diuretics such as furosemide or bumetanide [3,5,8,14,17,23,43,44]. These are mediated by the Na+/ Na + (Na+/Li +) exchange system [13] and by the so-called Na+-K + cotransport system [44] which is dependent on chloride [7,21] and blocked by loop diuretics such as furosemide or bumetanide [3,5,8,14,17,23,43,44].…”

Section: Introductionmentioning

confidence: 99%

“…However, Na + to K + stoichiometries varying between 1 : 1 and 1 : 5 have been reported [3,5,21,23,44]. Furthermore, furosemide-sensitive (FS) and chloride-dependent inward movements of K + have been described that occur in pure choline media in the absence of extracellular Na + (Na +) [5,8,21,30,43,44]. Thus, FS K + movements in human erythrocytes cannot simply be attributed to the action of a strictly coupled Na+-K + cotransport system.…”

Section: Introductionmentioning

confidence: 99%

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Furosemide-sensitive K+ (Rb+) transport in human erythrocytes: Modes of operation, dependence on extracellular and intracellular Na+, kinetics, pH dependency and the effect of cell volume and N-ethylmaleimide

Duhm

1987

J. Membrain Biol.

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The effect of extracellular and intracellular Na+ (Nao+, Nai+) on ouabain-resistant, furosemide-sensitive (FS) Rb+ transport was studied in human erythrocytes under varying experimental conditions. The results obtained are consistent with the view that a (1 Na+ + 1 K+ + 2 Cl-) cotransport system operates in two different modes: mode i) promoting bidirectional 1:1 (Na+-K+) cotransport, and mode ii) a Nao+-independent 1:1 ki+ exchange requiring Nai+ which, however, is not extruded. The activities of the two modes of operation vary strictly in parallel to each other among erythrocytes of different donors and in cell fractions of individual donors separated according to density. Rb+ uptake through Rbo+/Ki+ exchange contributes about 25% to total Rb+ uptake in 145 mM NaCl media containing 5 mM RbCl at normal Nai+ (pH 7.4). Na+-K+ cotransport into the cells occurs largely additive to K+/K+ exchange. Inward Na+-Rb+ cotransport exhibits a substrate inhibition at high Rbo+. With increasing pH, the maximum rate of cotransport is accelerated at the expense of K+/K+ exchange (apparent pK close to pH 7.4). The apparent KmRbo+ of Na+-K+ cotransport is low (2 mM) and almost independent of pH, and high for K+/K+ exchange (10 to 15 mM), the affinity increasing with pH. The two modes are discussed in terms of a partial reaction scheme of (1 Na+ + 1 K+ + 2 Cl-) cotransport with ordered binding and debinding, exhibiting a glide symmetry (first on outside = first off inside) as proposed by McManus for duck erythrocytes (McManus, T.J., 1987, Fed. Proc., in press). N-ethylmaleimide (NEM) chemically induces a Cl--dependent K+ transport pathway that is independent of both Nao+ and Nai+. This pathway differs in many properties from the basal, Nao+-independent K+/K+ exchange active in untreated human erythrocytes at normal cell volume. Cell swelling accelerates a Nao+-independent FS K+ transport pathway which most probably is not identical to basal K+/K+ exchange. Ko+ less than Nao+ less than Lio+ less than Mgo2+ reduce furosemide-resistant Rb+ inward leakage relative to cholineo+.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Furosemide-sensitive K+ (Rb+) transport in human erythrocytes: Modes of operation, dependence on extracellular and intracellular Na+, kinetics, pH dependency and the effect of cell volume and N-ethylmaleimide

Duhm

1987

J. Membrain Biol.

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“…Because of low Cl affinity, an increase in external Cl from 100 to 150 mM can stimulate bumetanide-sensitive K influx. Indeed, three other groups have reported that NaK2Cl cotransport-mediated K influx in human erythrocytes was 50-80% higher at an external Cl of 150 mM compared with the flux at an external Cl of 100 mM (23)(24)(25). Thus, most of the difference in baseline bumetanide-sensitive K influx with the two methods can be explained by the difference in external Cl concentrations.…”

Section: Resultsmentioning

confidence: 95%

Urea inhibits NaK2Cl cotransport in human erythrocytes.

Lim¹,

Gasson²,

Kaji³

1995

J. Clin. Invest.

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We examined the effect of urea on NaK2Cl cotransport in human erythrocytes. In erythrocytes from nine normal subjects, the addition of 45 mM urea, a concentration commonly encountered in uremic subjects, inhibited NaK2CI cotransport by 33±7%. Urea inhibited NaK2Cl cotransport reversibly, and in a concentration-dependent fashion with half-maximal inhibition at 63± 10 mM. Acute cell shrinkage increased, and acute cell swelling decreased NaK2Cl cotransport in human erythrocytes. Okadaic acid (OA), a specific inhibitor of protein phosphatase 1 and 2A, increased NaK2CI cotransport by nearly 80%, suggesting an important role for these phosphatases in the regulation of NaK2Cl cotransport. Urea inhibited bumetanide-sensitive K influx even when protein phosphatases were inhibited with OA, suggesting that urea acted by inhibiting a kinase. In cells subjected to shrinking and OA pretreatment, maneuvers expected to increase the net phosphorylation, urea inhibited cotransport only minimally, suggesting that urea acted by causing a net dephosphorylation of the cotransport protein, or some key regulatory protein. The finding that concentrations of urea found in uremic subjects inhibited NaK2Cl cotransport, a widespread transport pathway with important physiological functions, suggests that urea is not only a marker for accumulation of other uremic toxins, but may be a significant uremic toxin itself. (J. Clin. Invest. 1995. 96:2126-2132

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“…Although the efficacy of furosemide to inhibit K+ effilux in a SO42-medium was not tested, it is predicted that the failure to find a decrease in the efflux rate (as with NO3) reflects a change in the diureticinsensitive moiety. This serves as a reminder that the choice of replacement anions is very important where the aim is to identify Na+-K+-Cl-co-transport (see Chipperfield, 1985).…”

Section: Discussionmentioning

confidence: 99%

EVIDENCE FOR FUROSEMID E‐SENSITIVE Na⁺‐K⁺‐Cl^#x2212; CO‐TRANSPORT IN LACTATING RAT MAMMARY TISSUE

Shennan

1989

Exp Physiol

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SUMMARYThe transport of K+ (using 86Rb as tracer) by lactating rat mammary tissue slices has been studied in order to seek evidence for Na+-K+-Cl-co-transport. Potassium transport was inhibited by furosemide; the locus of inhibition was at a site other than the Na+: K+ pump.Replacing medium Cl-with NO3 reduced the bidirectional movement of K+; moreover, furosemide was without effect in a Cl--free medium. Sodium replacement by N-methyl-Dglucamine acted to reduce the loop diuretic-sensitive component of K+ uptake whilst concomitantly increasing K+ influx via an ouabain-and furosemide-resistant pathway. Potassium efflux was found to be transiently stimulated by Na+ ions; this was attenuated by furosemide. Potassium egress was markedly increased via a furosemide-insensitive pathway when salicylate was used to replace Cl-. The results are consistent with furosemide-sensitive Na+-K+-Cl-co-transport.

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Influence of loop diuretics and anions on passive potassium influx into human red cells.

Cited by 13 publications

References 29 publications

Furosemide-sensitive K+ (Rb+) transport in human erythrocytes: Modes of operation, dependence on extracellular and intracellular Na+, kinetics, pH dependency and the effect of cell volume and N-ethylmaleimide

Furosemide-sensitive K+ (Rb+) transport in human erythrocytes: Modes of operation, dependence on extracellular and intracellular Na+, kinetics, pH dependency and the effect of cell volume and N-ethylmaleimide

Urea inhibits NaK2Cl cotransport in human erythrocytes.

EVIDENCE FOR FUROSEMID E‐SENSITIVE Na⁺‐K⁺‐Cl^#x2212; CO‐TRANSPORT IN LACTATING RAT MAMMARY TISSUE

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Influence of loop diuretics and anions on passive potassium influx into human red cells.

Cited by 13 publications

References 29 publications

Furosemide-sensitive K+ (Rb+) transport in human erythrocytes: Modes of operation, dependence on extracellular and intracellular Na+, kinetics, pH dependency and the effect of cell volume and N-ethylmaleimide

Furosemide-sensitive K+ (Rb+) transport in human erythrocytes: Modes of operation, dependence on extracellular and intracellular Na+, kinetics, pH dependency and the effect of cell volume and N-ethylmaleimide

Urea inhibits NaK2Cl cotransport in human erythrocytes.

EVIDENCE FOR FUROSEMID E‐SENSITIVE Na+‐K+‐Cl#x2212; CO‐TRANSPORT IN LACTATING RAT MAMMARY TISSUE

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EVIDENCE FOR FUROSEMID E‐SENSITIVE Na⁺‐K⁺‐Cl^#x2212; CO‐TRANSPORT IN LACTATING RAT MAMMARY TISSUE