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J Neurosci. 1999 Jun 15;19(12):4695-704.
A furosemide-sensitive K+-Cl- cotransporter counteracts intracellular Cl- accumulation and depletion in cultured rat midbrain neurons.

Jarolimek W, Lewen A, Misgeld U.

I. Physiologisches Institut der Universitat Heidelberg, D-69120 Heidelberg, Germany.

Efficacy of postsynaptic inhibition through GABAA receptors in the mammalian brain depends on the maintenance of a Cl- gradient for hyperpolarizing Cl- currents. We have taken advantage of the reduced complexity under which Cl- regulation can be investigated in cultured neurons as opposed to neurons in other in vitro preparations of the mammalian brain. Tightseal whole-cell recording of spontaneous GABAA receptor-mediated postsynaptic currents suggested that an outward Cl- transport reduced dendritic [Cl-]i if the somata of cells were loaded with Cl- via the patch pipette. We determined dendritic and somatic reversal potentials of Cl- currents induced by focally applied GABA to calculate [Cl-]i during variation of [K+]o and [Cl-] in the patch pipette. [Cl-]i and [K+]o were tightly coupled by a furosemide-sensitive K+-Cl- cotransport. Thermodynamic considerations excluded the significant contribution of a Na+-K+-Cl- cotransporter to the net Cl- transport. We conclude that under conditions of normal [K+]o the K+-Cl- cotransporter helps to maintain [Cl-]i at low levels, whereas under pathological conditions, under which [K+]o remains elevated because of neuronal hyperactivity, the cotransporter accumulates Cl- in neurons, thereby further enhancing neuronal excitability.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10366603&dopt=Abstract

J Membr Biol. 1984;82(2):167-78.
Thiol-dependent passive K+Cl- transport in sheep red blood cells: VI. Functional heterogeneity and immunologic identity with volume-stimulated K+(Rb+) fluxes.

Lauf PK.

Ouabain-resistant (OR), volume- or N-ethylmaleimide (NEM)-stimulated K+(Rb+)Cl- fluxes were measured in low-K+ sheep red cells and found to be functionally separate but immunologically similar. In anisosmotic solutions both K+ effluxes and Rb+ influxes of NEM-treated and control cells were additive. In contrast to the NEM-stimulated K+Cl- flux, metabolic depletion did not reduce K+Cl- flux of normal or swollen cells. The anion preference of OR K+ efflux in NEM-treated cells was Br- greater than Cl- greater than HCO3- = F- much greater than I- = NO3- = CNS-, and hence consistent with a reported Br- greater than Cl- greater than NO3- sequence of the volume-dependent K+Cl- transport. Alloimmune anti-L1 antibodies known to decrease passive K+ fluxes in low K+ cells reduced by 51% both volume- and NEM-stimulated, furosemide-sensitive Rb+Cl- fluxes suggesting their immunologic identity, a conclusion also supported by anti-L1 absorption studies. Since pretreatment with anti-L1 prevented the activation of Rb+ influx by NEM, and the impermeant glutathionmaleimide-I did not stimulate Rb+Cl- influx, the NEM reactive SH groups must be located apart from the L1 antigen either within the membrane or on its cytoplasmic face. A model is proposed consisting of a K+Cl- transport path(s) regulated by a protein with two functional subunits or domains: a chemically (Cs) and a volume (Vs)-stimulated domain, both interfacing with the L1 surface antigen. Attachment of alloanti-L1 from the outside reduces K+Cl- transport stimulated through Cs by NEM or Vs by cell swelling.

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J Lab Clin Med. 1986 Feb;107(2):176-84.
Response of the renal K+-conserving mechanism to kaliuretic stimuli: evidence for a direct kaliuretic effect by furosemide.

Tannen RL, Gerrits L.

Isolated perfused kidneys from rats given a K+-free diet for 3 days demonstrate striking renal K+ conservation by a mechanism that is independent of perfusate and renal tissue K+, aldosterone, urine pH, urine flow, and sodium and anion excretion. To examine the effect of several kaliuretic stimuli on this intrinsic renal K+-conserving mechanism, kidneys from K+-depleted rats perfused with 3.5 mmol/L K+ were subjected to an experimental maneuver after 45 minutes of perfusion under normal conditions. Fractional potassium excretion (FEK) remained stable in time controls during a subsequent 45 minutes of perfusion. Acidification of the perfusate to pH 6.96 by addition of HCI had no significant effect on FEK. Alkalinization to pH 7.7 by either addition of NaHCO3 or a reduction in PCO2 resulted in significant kaliuresis (FEK 26% vs. 15%), which appeared to be a direct result of systemic alkalinization. Addition of Na2SO4 to the perfusate also produced significant kaliuresis (FEK 29%), which could not be dissociated from the magnitude of the natriuresis. Although both alkalosis and sulfate increased K+ excretion by depleted kidneys, FEK was much lower than with kidneys from normal rats perfused at pH 7.4 (FEK 51%). Thus the intrinsic renal K+-conserving mechanism dramatically diminishes the kidneys' kaliuretic potency and probably accounts for the blunted kaliuretic effect of these stimuli during K+ depletion in vivo. An increase in sodium excretion and urine flow rate achieved by lowering the perfusate albumin concentration, increasing the perfusate pressure, or adding the diuretics hydrochlorothiazide and furosemide resulted in significant kaliuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

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