Role of F-actin in the activation of Na+-K+-Cl- cotransport by forskolin and vasopressin in mouse kidney cultured thick ascending limb cells

M. S. Wu, M. Bens, F. Cluzeaud, A. Vandewalle

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The influence of microtubules and F-actin on Na+-K+-Cl- cotransport was investigated in cultured cells derived from outer-medullary thick ascending limb tubules microdissected from the mouse kidney. The cultured cells contained Tamm-Horsfall protein, produced cAMP in response to dD-arginine vasopressin (dD-AVP), isoproterenol, prostaglandin E2 and forskolin (FK), and exhibited an ouabain-resistant furosemidesensitive (Or-Fs) component of 86Rb+ influx mediated by the Na+-K+-Cl- cotransporter. Both FK and dD-AVP stimulated the Or-Fs component of Rb+ influx. Neither agent altered the tubulin and cytokeratin networks nor the shape of the tight junction using a specific anti-ZO-1 antibody. In contrast, they did induce a marked redistribution of F-actin to the periphery of the cells delineating the tight junctions. Preincubation of the cells with nocodazole, to disrupt microtubules, did not alter the FK-or dD-AVP-elicited Or-Fs Rb+ influx. In contrast, phalloidin and NBD-phallicidin, which stabilize F-actin, markedly impaired the stimulation of Na+-K+-Cl- cotransport by FK or dD-AVP, without affecting the Na+-K+ ATPase pumps and the rate constant of 36Cl- and 86Rb+ efflux. These results strongly suggested that cAMP-stimulated Na+-K+-Cl- cotransport is linked to F-actin in renal TAL cells.

Original languageEnglish
Pages (from-to)323-336
Number of pages14
JournalThe Journal of Membrane Biology
Issue number3
Publication statusPublished - Dec 1994
Externally publishedYes



  • cAMP
  • Cytoskeleton
  • F-actin
  • Kidney
  • Microtubules
  • Potassium transport

ASJC Scopus subject areas

  • Physiology
  • Cell Biology
  • Biophysics

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