Literature DB >> 7407122

Electrically silent cotransport on Na+, K+ and Cl- in Ehrlich cells.

P Geck, C Pietrzyk, B C Burckhardt, B Pfeiffer, E Heinz.   

Abstract

A cotransport system for Na+, K+ and Cl- in Ehrlich cells is described. It is insensitive towards ouabain but specifically inhibited by furosemide and other 'high ceiling' diuretics at concentrations which do not affect other pathways of the ions concerned. As the furosemide-sensitive fluxes of these ions are no affected by changes in membrane potential, and as their complete inhibition by furosemide does not appreciably alter the membrane potential, they appear to be electrically silent. Application of the pulse-response methods in terms of irreversible thermodynamics reveals tight coupling between the furosemide-sensitive flows of Na+, K+ and Cl- (q close to unity for all three combinations) at a stoichiometry of 1: 1 : 2. The site for each of the ions appears to be rather specific: K+ can be replaced by Rb+ but not by other cations tested whereas Cl- can be poorly replaced by Br- but not by NO(-)3, in contradistinction to the Cl(-)-OH- exchange system. The cotransport system appears to function in cell volume regulatin as it tends to make the cell swell, thus counteracting the shrinking effect of the ouabain-sensitive (Na+, K+) pump. The experiments presented could not clarify whether the cotransport process is a primary or secondary active one; while incongruence between transport and conjugated driving force seems to indicate primary active transport, it is very unlikely that hydrolysis of ATP supplies energy for the transport process, since thre is not stimulation of ATP turnover observable under operation of the cotransport system.

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Year:  1980        PMID: 7407122     DOI: 10.1016/0005-2736(80)90446-0

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


  128 in total

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Journal:  Pflugers Arch       Date:  2003-05-09       Impact factor: 3.657

Review 2.  Stimulus-secretion coupling: cytoplasmic calcium signals and the control of ion channels in exocrine acinar cells.

Authors:  O H Petersen
Journal:  J Physiol       Date:  1992-03       Impact factor: 5.182

3.  Contributions of secondary active transport processes to membrane potentials.

Authors:  L G Gordon; A D Macknight
Journal:  J Membr Biol       Date:  1991-03       Impact factor: 1.843

4.  Molecular determinants of hyperosmotically activated NKCC1-mediated K+/K+ exchange.

Authors:  Kenneth B Gagnon; Eric Delpire
Journal:  J Physiol       Date:  2010-06-07       Impact factor: 5.182

Review 5.  Physiology of SLC12 transporters: lessons from inherited human genetic mutations and genetically engineered mouse knockouts.

Authors:  Kenneth B Gagnon; Eric Delpire
Journal:  Am J Physiol Cell Physiol       Date:  2013-01-16       Impact factor: 4.249

6.  Regulation of synaptic transmission at the photoreceptor terminal: a novel role for the cation-chloride co-transporter NKCC1.

Authors:  Wen Shen; Lauren A Purpura; Baoqin Li; Changlong Nan; Irene J Chang; Harris Ripps
Journal:  J Physiol       Date:  2012-10-22       Impact factor: 5.182

Review 7.  Physiology and pathophysiology of SLC12A1/2 transporters.

Authors:  Nicolas Markadieu; Eric Delpire
Journal:  Pflugers Arch       Date:  2013-10-06       Impact factor: 3.657

8.  Volume-regulatory K+ efflux during concentrative uptake of alanine in isolated rat hepatocytes.

Authors:  L O Kristensen; M Folke
Journal:  Biochem J       Date:  1984-07-01       Impact factor: 3.857

9.  Endogenous Na(+)-K+ (or NH4+)-2Cl- cotransport in Rana oocytes; anomalous effect of external NH4+ on pHi.

Authors:  E Keicher; R Meech
Journal:  J Physiol       Date:  1994-02-15       Impact factor: 5.182

10.  Phorbol ester inhibits furosemide-sensitive potassium transport in BALB/c 3T3 preadipose cells.

Authors:  T G O'Brien; K Krzeminski
Journal:  Proc Natl Acad Sci U S A       Date:  1983-07       Impact factor: 11.205

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