The Na−K−2Cl cotransport system

Geck, Peter; Heinz, Erich

doi:10.1007/bf01925787

Cited by 185 publications

(130 citation statements)

References 87 publications

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“…This mechanism has been described in Ehrlich ascites tumour cells (Geck & Heinz, 1986), the thick ascending limb of Henle's loop (Greger & Schlatter, 1981) and in the intestine of the flounder (Musch et al 1982). A prerequisite of this transport mechanism is the luminal concentration of potassium.…”

Section: Na-k-2ct Co-transportmentioning

confidence: 86%

Mechanism of electrically silent Na and Cl transport across the rumen epithelium of sheep

Martens

Gäbel²,

Strozyk³

1991

Experimental Physiology

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SUMMARYThis study was designed to study the mechanism of electroneutral Na and Cl transport across the isolated rumen epithelium of sheep. Net sodium transport (5 75 + 0-35 ,uequiv cm-2 h-1) was significantly higher than the short-circuit current (0 95 + 0-08 ,uequiv cm-2 h-'). Both, net sodium and net chloride transport were markedly reduced by replacement of chloride, bicarbonate and sodium, respectively, but were not changed by the absence of mucosal potassium. Net sodium and net chloride absorption was significantly decreased by 10 mmamiloride. Mucosal addition of bumetanide, furosemide, hydrochlorothiazide or low concentrations of amiloride (< 0 1 mM) did not change sodium fluxes. These results provide compelling evidence consistent with the presence of Na-H exchange as the predominant electroneutral mechanism for transepithelial sodium movement. The ion replacement studies and data from literature suggest that the Na-H exchange is working in parallel with a Cl-HCO3 exchange although luminal addition of DIDS (4,4'diisothiocyanatostilbene-2,2'-disulphonate, 1 mM) did not significantly influence Cl transport.

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Section: Na-k-2ct Co-transportmentioning

confidence: 86%

Mechanism of electrically silent Na and Cl transport across the rumen epithelium of sheep

Martens

Gäbel²,

Strozyk³

1991

Experimental Physiology

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“…had no influence on the biphasic Glu response; in particular, no shift of Er was observed. The loop diuretic furosemide is well-established as an inhibitor of the Na+-K+-2Cl-co-transport system (Geck & Heinz, 1986). It has also been reported that furosemide inhibits neurotransmitter-activated chloride currents: GABA responses in frog spinal motoneurones (Nicoll, 1978) and acetylcholine responses in molluscan neurones (Katchman & Zeimal, 1982).…”

Section: Ionic Basis Of Glu Responsementioning

confidence: 99%

Different types of glutamate receptors in isolated and identified neurones of the mollusc Planorbarius corneus.

Bolshakov

Gapon

1991

The Journal of Physiology

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SUMMARY1. The membrane currents evoked by glutamate agonists on isolated and identified neurones of molluscan pedal ganglia were investigated using the voltage clamp technique.2. The fast chloride current (Er (reversal potential) =-41 mV) evoked in a Ped-9 neurone by application of glutamate, quisqualate and ibotenic acid could be blocked by furosemide (0-1 mM). The slow potassium current (Er = -85 mV) evoked in Ped-8 and Ped-9 neurones by glutamate, quisqualate and kainate could be blocked by tetraethylammonium (50 /M).3. N-Methyl-D-aspartate (NMDA) and a-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) failed to induce a response in neurones studies.4. The spider venoms argiopine and argiopinine III (50-500 nM) selectively inhibited quisqualate-induced potassium current, but had no influence on glutamate-, ibotenate-or quisqualate-induced chloride and kainate-induced potassium currents. Glutamate-induced potassium current was partially inhibited by argiopine and argiopinine III.5. The existence of several types of distinct glutamate receptors was confirmed in cross-desensitization experiments, and a lack of interaction was observed between quisqualate and kainate.6. Potassium currents induced both by quisqualate and kainate strongly depended on temperature and could be blocked by pertussis toxin. Intracellular injection of the calcium chelator, EGTA, did not affect quisqualate and kainate responses.7. In neurones loaded with non-hydrolysable GTP analogues, GTP-y-S (guanosine-5'-O-(3-thio)triphosphate) or GppNHp (5'-guanylylimidodiphosphate), the potassium current was gradually induced in the absence of agonists. As this current progressed, the magnitude of the glutamate-or kainate-evoked current transients became smaller and finally negligible. The GTP-y-S-induced current was not inhibited by argiopine.

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“…The suitability of Rb as a substitute for K has 496 JOINER been well documented for ion transport studies in the human red cell (14)(15)(16). Heparinized blood was obtained with informed consent under a protocol approved by the Institutional Review Board of the University of Alabama at Birmingham, from normal white volunteers (aged 22-50 yr, median 27 yr) or from ambulatory C F patients (aged 1 1-37 yr, median 16 yr) who were not taking digitalis derivatives or diuretics.…”

Section: Methodsmentioning

confidence: 99%

Kinetic Parameters of Rubidium Transport Pathways Are Normal in Cystic Fibrosis Red Cells

Joiner

1988

Pediatr Res

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ABSTRACT. The abnormalities in ion transport in cystic fibrosis (CF) respiratory and sweat duct epithelia have prompted Studies of ion permeability in CF red blood cells (RBC) although previous reports have been contradictory. In this study, the kinetic characteristics of the three major cation transport systems in RBC were evaluated by measuring rubidium (Rb) uptake at various external Rb concentrations. The maximal velocity and affinity for external Rb (KH) of the NaK pump were normal in CF RBC, as were the maximal velocity and K, for Rb of the NaK cotransport system. Residual (ouabain and bumetanide insensitive) Rb uptake, and steady state RBC Na and K contents were also normal. These data indicate the NaK pump and cotransport system do not exhibit primary or secondary perturbations in CF RBC, and suggest that the noncarrier-mediated membrane permeability to cations is also normal in these cells. (Pediatr Res 24: 495-498, 1988) Abbreviations CF, cystic fibrosis RBC, red blood cell V , , maximal velocity K, Rb, external K or Rb PBS, phosphate-buffered saline OS, ouabain-sensitive Co, cotransport CF is an autosomal recessive disorder manifesting multiple exocrine abnormalities (1). The diagnostically important elevation of sweat chloride reflects malfunctioning of the salt resorbing mechanisms of sweat duct epithelium. Recent work has indicated that the basis of this dysfunction is low C1 permeability of the apical membrane of the ductal epithelial cells (2). Respiratory epithelia share this defect (3), which appears in these cells to arise from abnormalities of the adrenergic regulatory mechanisms of the C1 channel (4-6). Other recent studies of CF respiratory epithelia have also shown increased permeability of the apical membrane to Na, accompanied by elevated Na pump rates at the basolateral membrane, with increased numbers of [3H]ouabain binding sites and ouabain-inhibitable oxygen consumption (7). These findings suggest that, in addition to the C1 channel,

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The Na−K−2Cl cotransport system

Cited by 185 publications

References 87 publications

Mechanism of electrically silent Na and Cl transport across the rumen epithelium of sheep

Mechanism of electrically silent Na and Cl transport across the rumen epithelium of sheep

Different types of glutamate receptors in isolated and identified neurones of the mollusc Planorbarius corneus.

Kinetic Parameters of Rubidium Transport Pathways Are Normal in Cystic Fibrosis Red Cells

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