Inhibition of anion permeability by amphiphilic compounds in human red cell: Evidence for an interaction of niflumic acid with the band 3 protein

Cousin, J.; Motais, R

doi:10.1007/bf01961377

Cited by 88 publications

(32 citation statements)

References 54 publications

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“…The ICo of niflumic acid against Ic(Ca) in Xenopus oocytes was estimated to be 17 #iM (White & Aylwin, 1990) which is almost an order less potent than against STICs at IC5o of about 2.5 x 10-1 M (Hughes & Segawa, 1993). Also niflumic acid is a potent inhibitor (ICm of 6.3 x 10-7 M) of anion exchange in human red cells where it has been suggested that niflumic acid interacts with the band 3 protein (Cousin & Motais, 1979). It is interesting that many compounds that block chloride channels also inhibit anion transport in red blood cells (also see Cousin & Motais, 1982a,b).…”

Section: Discussionmentioning

confidence: 99%

Action of niflumic acid on evoked and spontaneous calcium‐activated chloride and potassium currents in smooth muscle cells from rabbit portal vein

Hogg

Wang

Large

1994

British J Pharmacology

124

122

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1 The action of niflumic acid was studied on spontaneous and evoked calcium-activated chloride (IC1(ca)) and potassium (IK(Ca)) currents in rabbit isolated portal vein cells.2 With the nystatin perforated patch technique in potassium-containing solutions at a holding potential of -77 mV (the potassium equilibrium potential), niflumic acid produced a concentrationdependent inhibition of spontaneous transient inward current (STIC, calcium-activated chloride current) amplitude. The concentration to reduce the STIC amplitude by 50% (ICM) was 3.6 x 10-6 M.3 At -77 mV holding potential, niflumic acid converted the STIC decay from a single exponential to 2 exponential components. In niflumic acid the fast component of decay was faster, and the slow component was slower than the control decay time constant. Increasing the concentration of niflumic acid enhanced the decay rate of the fast component and reduced the decay rate of the slow component. 4 The effect of niflumic acid on STIC amplitude was voltage-dependent and at -50 and + 50 mV the IC50 values were 2.3 X 10-6 M and 1.1 X 10-6 M respectively (cf. 3.6 x 10-6 M at -77 mV).5 In K-free solutions at potentials of -50 mV and + 50 mV, niflumic acid did not induce a dual exponential STIC decay but just increased the decay time constant at both potentials in a concentrationdependent manner.6 Niflumic acid, in concentrations up to 5 x 10-5 M, had no effect on spontaneous calcium-activated potassium currents.7 Niflumic acid inhibited noradrenaline-and caffeine-evoked IO(C.) with an ICM of 6.6 x 10-6 M, i.e. was less potent against evoked currents compared to spontaneous currents. In contrast niflumic acid (2 x 10-6 M-5 x 105 M) increased noradrenaline-and caffeine-induced I ). 8 The results are discussed with respect to the mechanism of block of ICl(Ca) by niflumic acid and its suitability as a pharmacological tool for assessing the role of Ic(cp) in physiological mechanisms.

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Section: Discussionmentioning

confidence: 99%

Action of niflumic acid on evoked and spontaneous calcium‐activated chloride and potassium currents in smooth muscle cells from rabbit portal vein

Hogg

Wang

Large

1994

British J Pharmacology

124

122

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“…This effect on chloride efflux has been described in sympathetic neurones where it was found that reduced extracellular chloride depleted intracellular chloride over time, or after repeated applications of GABA (Adams & Brown, 1975 Senktide and GABAA currents were blocked by the fenamates, niflumic and mefenamic acid. These drugs block anion transport (Cousin & Motais, 1979) and anion channels (White & Aylwin, 1990). Fenamates can also block cation conductances (Gogelein, Dahlem, Englert & Lang, 1990), but not cation transport (Cousin & Motais, 1979).…”

Section: Characterization Of Neuronesmentioning

confidence: 99%

“…These drugs block anion transport (Cousin & Motais, 1979) and anion channels (White & Aylwin, 1990). Fenamates can also block cation conductances (Gogelein, Dahlem, Englert & Lang, 1990), but not cation transport (Cousin & Motais, 1979). It is unlikely that the fenamates were blocking cation channels in the present study as fEPSPs in S-neurones were unaffected by these drugs.…”

Section: Characterization Of Neuronesmentioning

confidence: 99%

Contribution of chloride conductance increase to slow EPSC and tachykinin current in guinea‐pig myenteric neurones.

Bertrand

Galligan

1994

The Journal of Physiology

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1. Single electrode voltage clamp recordings were obtained from myenteric neurones of guinea-pig ileum in vitro. Slow excitatory postsynaptic currents (sEPSCs) were elicited by focal stimulation of interganglionic nerve strands in twenty-four of thirty neurones more than 30 min after impalement. In seventeen of twenty-four neurones, sEPSCs were associated with a conductance decrease and reversed polarity at -96 + 3 mV (near the reversal potential for potassium, EK); this response was due to inhibition of resting potassium conductance, gK. In seven of twenty-four neurones, there was either no net conductance change or a biphasic conductance change during the sEPSC; a reversal potential for peak currents could not be determined. 2. Application of senktide (3/uM), a neurokinin-3 receptor agonist, caused an inward current in forty-one of fifty-three neurones more than 30 min after impalement. In twenty of forty-one neurones, senktide-induced currents were due to inhibition of resting gK. In eleven of forty-one neurones there was either no net conductance change or a biphasic conductance change; a reversal potential for peak currents could not be determined. In ten out of forty-one neurones, senktide-induced currents were associated with a conductance increase (ginc); the estimated reversal potential was -17 + 3 mV.3. Application of forskolin (1 ,lM) caused an inward current that occluded the decrease in gK caused by senktide and the sEPSC. In neurones in which sESPCs and senktide responses were associated with an unclear or biphasic conductance change, forskolin did not reduce the peak current and residual currents were usually associated with a gin, 4. In neurones in which senktide-induced currents were associated with a gin, reducing extracellular Cl-to 13 mm reduced senktide-induced currents by 79%. Reducing extracellular Na+, or adding tetraethylammonium (TEA, 50 mM), cobalt (2 mM) or picrotoxin (30 ,lM) did not change senktide-induced currents. The chloride transport/ channel blockers niflumic acid and mefenamic acid (both at 100 /SM) blocked senktideinduced currents. It was concluded that senktide increases chloride conductance (gcl).5. Chord conductance measurements made between -70 and -90 mV during sEPSCs were used to determine the contribution of an increase in gcl to sEPSCs. These measurements indicated that the peak sEPSC is composed of a 90% decrease in g9 and a 10% increase in gcl. Similar data were obtained from measurements made during senktide responses.It was concluded that senktide-induced currents and sEPSCs are due to a concurrent decrease in g9 and an increase in gcl in a subset of myenteric neurones.

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“…Other inhibitors of some anion-transport systems were tested extracellularly: furosemide (up to 1 mM; see Burg, Stoner, Cardinal & Green, 1973), penicillin 297 D. CHESNO Y-MARCHAIS (sodium benzylpenicillinate, up to 10 mM; see Hochner, Spira & Werman, 1976) and niflumic acid (up to 20/SM; see Cousin & Motais, 1979) had no effect on the Cl-current. Higher doses of niflumic acid seemed toxic, inducing a large increase in membrane conductance.…”

Section: Effects Of Depolarizing Pre-pul8ebmentioning

confidence: 99%

Characterization of a chloride conductance activated by hyperpolarization in Aplysia neurones.

Chesnoy-Marchais¹

1983

The Journal of Physiology

102

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SUMMARY1. A voltage-clamp study was made of some properties of the non-synaptic hyperpolarization-activated C1-conductance recently described in Aplysia neurones loaded with Cl-ions (Chesnoy-Marchais, 1982). The experiments were performed on an identified family of neurones, which present cholinergic responses allowing an easy measurement of the equilibrium potentials of Cl-(EC1) and K+ ions (EK).2. The Cl-selectivity ofthe hyperpolarization-activated conductance was deduced from four observations: (1) the extrapolated reversal potential of the hyperpolarization-activated current, Er, was close to the reversal potential ofthe cholinergic Cl-response, which is the equilibrium potential for Cl-ions, EC1. 3. The steady-state Cl-conductance (ass) increases steeply with hyperpolarization.The kinetics of activation and deactivation are exponential and are characterized by the same voltage-dependent time constant (r), of the order of a few seconds or fractions of seconds. The curves g.8(V) and r( V) can both be fitted by a two-state model in which the rate constants are exponential functions of the membrane potential (e-fold change for 12-16 mV).4. The Cl-current is much more affected by changes of the intracellular Clconcentration than predicted simply from the change in Cl-driving force. Both the conductance and the time constant of activation are strongly modified. Modifications of the extracellular Cl-concentration do not always alter the amplitude of the hyperpolarization-activated Cl-current, but systematically affect its kinetics.5. The hyperpolarization-activated current is abolished after prolonged exposure of the cell to an artificial sea water where N03-ions replace Cl-ions, as well as after intracellular injections of N03-ions.6. Increasing the external pH shifts the g.(V) and r(V) curves to the left.Lowering the external pH has reverse but less pronounced effects. 7. In cells which were not loaded with Cl-ions and did not present the hyperpolarization-activated Cl-current, this current could be detected if the D. CHESNO Y-MARCHAIS hyperpolarizing jump was preceded by short depolarizing pulses. In cells which were loaded with Cl-ions, the Cl-current became larger after a short depolarizing pulse.In the presence of extracellular C02+ ions, depolarizing pulses no longer increased the Cl-current.8. The Cl-current is not affected by extracellularly applied DIDS (4,4'-diisothiocyano-2,2'-disulphonic acid stilbene), but is markedly reduced by intracellular injection of DIDS.9. Extracellular Cs+ ions, which have been reported to block some cationic hyperpolarization-activated inward currents, do not reduce the hyperpolarizationactivated Cl-current. High concentrations of Cs+ produce complex effects which are probably due to an increased synaptic activity, but the hyperpolarization-activatedCl-current persists after complete substitution of the extracellular and intracellular monovalent cations by Cs+.

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Inhibition of anion permeability by amphiphilic compounds in human red cell: Evidence for an interaction of niflumic acid with the band 3 protein

Cited by 88 publications

References 54 publications

Action of niflumic acid on evoked and spontaneous calcium‐activated chloride and potassium currents in smooth muscle cells from rabbit portal vein

Action of niflumic acid on evoked and spontaneous calcium‐activated chloride and potassium currents in smooth muscle cells from rabbit portal vein

Contribution of chloride conductance increase to slow EPSC and tachykinin current in guinea‐pig myenteric neurones.

Characterization of a chloride conductance activated by hyperpolarization in Aplysia neurones.

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