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dc.contributor.authorLayton, Anita T.en_US
dc.contributor.authorEdwards, Aurelieen_US
dc.contributor.authorVallon, Volkeren_US
dc.date.accessioned2020-02-25T22:13:10Z
dc.date.available2020-02-25T22:13:10Z
dc.date.issued2018-04-01
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000440942800013&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=6e74115fe3da270499c3d65c9b17d654
dc.identifier.citationAnita T Layton, Aurelie Edwards, Volker Vallon. 2018. "Renal potassium handling in rats with subtotal nephrectomy: modeling and analysis." American Journal of Physiology: Renal Physiology, Volume 314, Issue 4, pp. F643 - F657. https://doi.org/10.1152/ajprenal.00460.2017
dc.identifier.issn1931-857X
dc.identifier.issn1522-1466
dc.identifier.urihttps://hdl.handle.net/2144/39527
dc.description.abstractWe sought to decipher the mechanisms underlying the kidney's response to changes in K+ load and intake, under physiological and pathophysiological conditions. To accomplish that goal, we applied a published computational model of epithelial transport along rat nephrons in a sham rat, an uninephrectomized (UNX) rat, and a 5/6-nephrectomized (5/6-NX) rat that also considers adaptations in glomerular filtration rate and tubular growth. Model simulations of an acute K+ load indicate that elevated expression levels and activities of Na+/K+-ATPase, epithelial sodium channels, large-conductance Ca2+-activated K+ channels, and renal outer medullary K+ channels, together with downregulation of sodium-chloride cotransporters (NCC), increase K+ secretion along the connecting tubule, resulting in a >6-fold increase in urinary K+ excretion in sham rats, which substantially exceeds the filtered K+ load. In the UNX and 5/6-NX models, the acute K+ load is predicted to increase K+ excretion, but at significantly reduced levels compared with sham. Acute K+ load is accompanied by natriuresis in sham rats. Model simulations suggest that the lesser natriuretic effect observed in the nephrectomized groups may be explained by impaired NCC downregulation in these kidneys. At a single-nephron level, a high K+ intake raises K+ secretion along the connecting tubule and reabsorption along the collecting duct in sham, and even more in UNX and 5/6-NX. However, the increased K+ secretion per tubule fails to sufficiently compensate for the reduction in nephron number, such that nephrectomized rats have an impaired ability to excrete an acute or chronic K+ load.en_US
dc.description.sponsorshipThis research was supported by the Department of Veterans Affairs (V. Vallon), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Grants R01-DK-112042 (V. Vallon) and R01-DK-106102 (A. T. Layton and V. Vallon), and University of Alabama at Birmingham-University of California San Diego O'Brien Center for Acute Kidney Injury Research (NIDDK Grant P30-DK-079337; V. Vallon). (Department of Veterans Affairs; R01-DK-112042 - National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); R01-DK-106102 - National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); P30-DK-079337 - University of Alabama at Birmingham-University of California San Diego O'Brien Center for Acute Kidney Injury Research (NIDDK Grant))en_US
dc.format.extentF643 - F657 (15)en_US
dc.languageEnglish
dc.publisherAMER PHYSIOLOGICAL SOCen_US
dc.relation.ispartofAmerican Journal of Physiology: Renal Physiology
dc.subjectScience & technologyen_US
dc.subjectLife sciences & biomedicineen_US
dc.subjectPhysiologyen_US
dc.subjectUrology & nephrologyen_US
dc.subjectEpithelial transporten_US
dc.subjectHomeostasisen_US
dc.subjectKaliuresisen_US
dc.subjectNatriuresisen_US
dc.subjectRemnant kidneyen_US
dc.subjectAdaptation, physiologicalen_US
dc.subjectAnimalsen_US
dc.subjectEpithelial cellsen_US
dc.subjectEpithelial sodium channelsen_US
dc.subjectGlomerular filtration rateen_US
dc.subjectKidneyen_US
dc.subjectLarge-conductance calcium-activated potassium channelsen_US
dc.subjectModels, animalen_US
dc.subjectModels, biologicalen_US
dc.subjectNatriuresisen_US
dc.subjectNephrectomyen_US
dc.subjectPotassiumen_US
dc.subjectPotassium, dietaryen_US
dc.subjectRatsen_US
dc.subjectRenal eliminationen_US
dc.subjectRenal reabsorptionen_US
dc.subjectSodium-potassium-exchanging ATPaseen_US
dc.subjectSolute carrier Family 12, Member 3en_US
dc.subjectTime factorsen_US
dc.subjectPhysiologyen_US
dc.subjectMedical physiologyen_US
dc.titleRenal potassium handling in rats with subtotal nephrectomy: modeling and analysisen_US
dc.typeArticleen_US
dc.description.versionAccepted manuscripten_US
dc.identifier.doi10.1152/ajprenal.00460.2017
pubs.elements-sourceweb-of-scienceen_US
pubs.notesEmbargo: 12 monthsen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Engineeringen_US
pubs.organisational-groupBoston University, College of Engineering, Department of Biomedical Engineeringen_US
pubs.publication-statusPublisheden_US
dc.identifier.mycv318304


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