title: Absence of KCNQ1-dependent K+ fluxes in proximal tubular cells of frog kidney.
abstract: The present study was designed to investigate the functional significance of KCNQ1-mediated K+ secretory fluxes in proximal tubular cells of the frog kidney. To this end, we investigated the effects on rapid depolarization and slow repolarization of the peritubular membrane potential after luminal addition of L-phenylalanine or L-alanine plus/minus KCNQ1 channel blockers. Perfusing the lumen with 10 mmol/L L-phenylalanine plus/minus luminal 293B, a specific blocker of KCNQ1, did not modify the rapid depolarization and the rate of slow repolarization. Perfusing the lumen with 10 mmol/L L-alanine plus/minus luminal HMR-1556, a more potent KCNQ1 channel blocker, did not also alter the rapid depolarization and the rate of slow repolarization. Pretreatment (1 h) of the lumen with HMR-1556 also failed to modify rapid depolarization and rate of slow repolarization upon luminal 10 mmol/L L-alanine. Perfusing the lumen with 1 mmol/L L-alanine plus/minus luminal HMR-1556 did not change the rapid depolarization and the rate of slow repolarization. The pretreatment (1 h) with luminal HMR-1556 did not modify the rapid depolarization and the rate of slow repolarization upon luminal 1 mmol/L L-alanine. The pretreatment (1 h) of the lumen with HMR-1556 did not change transference number for K+ of peritubular cell membrane. Finally, luminal barium blunted the rapid depolarization upon application of luminal 1 mmol/L L-alanine. RT-PCR showed that KCNQ1 mRNA was not expressed in frog kidney. In conclusion, the KCNQ1-dependent K+ secretory fluxes are absent in proximal tubule of frog kidney.
authors.affiliation: Department of Pathological Physiology, Medical Faculty, Dr Subotica 1/II, 11000 Belgrade, Serbia. dcemeri@afrodita.rcub.bg.ac.yu
authors.forename: Dusan
authors.initials: D
authors.lastname: Cemerikic
authors.forename: Jelena
authors.initials: J
authors.lastname: Nesovic-Ostojic
authors.forename: Dusan
authors.initials: D
authors.lastname: Popadic
authors.forename: Aleksandra
authors.initials: A
authors.lastname: Knezevic
authors.forename: Simon
authors.initials: S
authors.lastname: Dragovic
authors.forename: Aleksandar
authors.initials: A
authors.lastname: Milovanovic
authors.forename: Jovica
authors.initials: J
authors.lastname: Milovanovic
mesh_terms: D000409:Alanine / Q000378:metabolism; D000818:Animals; D001464:Barium / Q000378:metabolism; D002839:Chromans / Q000494:pharmacology; D066298:In Vitro Techniques; D051657:KCNQ1 Potassium Channel / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D008564:Membrane Potentials; D010477:Perfusion; D010649:Phenylalanine / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D011893:Rana esculenta / Q000235:genetics / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D002839:Chromans; C420023:HMR 1556; D051657:KCNQ1 Potassium Channel; D026902:Potassium Channel Blockers; D012333:RNA, Messenger; D013449:Sulfonamides; C103474:6-cyano-4-(N-ethylsulfonyl-N-methylamino)-3-hydroxy-2,2-dimethylchromane; D001464:Barium; D010649:Phenylalanine; D012964:Sodium; D000409:Alanine; D011188:Potassium