Maxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet

dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorBailey, M. A.
dc.creatorCantone, A.
dc.creatorYan, Q.
dc.creatorMacGregor, G. G.
dc.creatorLeng, Q.
dc.creatorAmorim, J. B O
dc.creatorWang, T.
dc.creatorHebert, S. C.
dc.creatorGiebisch, G.
dc.creatorMalnic, G.
dc.date2014-05-27T11:21:55Z
dc.date2016-10-25T18:22:28Z
dc.date2014-05-27T11:21:55Z
dc.date2016-10-25T18:22:28Z
dc.date2006-07-12
dc.date.accessioned2017-04-06T01:19:41Z
dc.date.available2017-04-06T01:19:41Z
dc.identifierKidney International, v. 70, n. 1, p. 51-59, 2006.
dc.identifier0085-2538
dc.identifier1523-1755
dc.identifierhttp://hdl.handle.net/11449/69001
dc.identifierhttp://acervodigital.unesp.br/handle/11449/69001
dc.identifier10.1038/sj.ki.5000388
dc.identifier2-s2.0-33745683633
dc.identifierhttp://dx.doi.org/10.1038/sj.ki.5000388
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/890300
dc.descriptionType II Bartter's syndrome is a hereditary hypokalemic renal salt-wasting disorder caused by mutations in the ROMK channel (Kir1.1; Kcnj1), mediating potassium recycling in the thick ascending limb of Henle's loop (TAL) and potassium secretion in the distal tubule and cortical collecting duct (CCT). Newborns with Type II Bartter are transiently hyperkalemic, consistent with loss of ROMK channel function in potassium secretion in distal convoluted tubule and CCT. Yet, these infants rapidly develop persistent hypokalemia owing to increased renal potassium excretion mediated by unknown mechanisms. Here, we used free-flow micropuncture and stationary microperfusion of the late distal tubule to explore the mechanism of renal potassium wasting in the Romk-deficient, Type II Bartter's mouse. We show that potassium absorption in the loop of Henle is reduced in Romk-deficient mice and can account for a significant fraction of renal potassium loss. In addition, we show that iberiotoxin (IBTX)-sensitive, flow-stimulated maxi-K channels account for sustained potassium secretion in the late distal tubule, despite loss of ROMK function. IBTX-sensitive potassium secretion is also increased in high-potassium-adapted wild-type mice. Thus, renal potassium wasting in Type II Bartter is due to both reduced reabsorption in the TAL and K secretion by max-K channels in the late distal tubule. © 2006 International Society of Nephrology.
dc.languageeng
dc.relationKidney International
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectIberiotoxin
dc.subjectMaxi-K channel
dc.subjectMicroperfusion
dc.subjectMicropuncture
dc.subjectPotassium adaptation
dc.subjectiberiotoxin
dc.subjectpotassium
dc.subjectpotassium channel
dc.subjectpotassium channel Kir1.1
dc.subjectprotein kcnj1
dc.subjectunclassified drug
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectBartter syndrome
dc.subjectcontrolled study
dc.subjectflow measurement
dc.subjectgene mutation
dc.subjectgenetic disorder
dc.subjectHenle loop
dc.subjecthigh potassium intake
dc.subjecthypokalemia
dc.subjectkidney distal tubule
dc.subjectkidney tubule absorption
dc.subjectmouse
dc.subjectnonhuman
dc.subjectpotassium excretion
dc.subjectpotassium transport
dc.subjectpriority journal
dc.subjectsalt losing nephritis
dc.subjectwild type
dc.subjectAdaptation, Physiological
dc.subjectAnimals
dc.subjectBartter Syndrome
dc.subjectBiological Transport
dc.subjectDiet
dc.subjectDisease Models, Animal
dc.subjectHypokalemia
dc.subjectKidney Tubules, Distal
dc.subjectLarge-Conductance Calcium-Activated Potassium Channels
dc.subjectLoop of Henle
dc.subjectMice
dc.subjectMice, Mutant Strains
dc.subjectPeptides
dc.subjectPotassium
dc.subjectPotassium Channels, Inwardly Rectifying
dc.subjectPotassium, Dietary
dc.titleMaxi-K channels contribute to urinary potassium excretion in the ROMK-deficient mouse model of Type II Bartter's syndrome and in adaptation to a high-K diet
dc.typeOtro


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