ISSN:
1432-1424
Keywords:
Cytoskeleton
;
F-actin
;
Microtubules
;
Potassium transport
;
cAMP
;
Kidney
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Chemistry and Pharmacology
Notes:
Abstract 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00233439
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