Angiotensin II and hypertonicity modulate proximal tubular aquaporin 1 expression

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dc.contributor.authorBouley, Richard
dc.contributor.authorPalomino, Zaira [UNIFESP]
dc.contributor.authorTang, Shiow-Shih
dc.contributor.authorNunes, Paula
dc.contributor.authorKobori, Hiroyuki
dc.contributor.authorLu, Hua A.
dc.contributor.authorShum, Winnie W.
dc.contributor.authorSabolic, Ivan
dc.contributor.authorBrown, Dennis
dc.contributor.authorIngelfinger, Julie R.
dc.contributor.authorJung, Flavia F.
dc.contributor.institutionHarvard Univ
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionTulane Univ
dc.contributor.institutionInst Med Res & Occupat Hlth
dc.contributor.institutionMassachusetts Gen Hosp
dc.contributor.institutionGeorgetown Univ
dc.date.accessioned2016-01-24T13:58:56Z
dc.date.available2016-01-24T13:58:56Z
dc.date.issued2009-12-01
dc.description.abstractBouley R, Palomino Z, Tang S-S, Nunes P, Kobori H, Lu HA, Shum WW, Sabolic I, Brown D, Ingelfinger JR, Jung FF. Angiotensin II and hypertonicity modulate proximal tubular aquaporin 1 expression. Am J Physiol Renal Physiol 297: F1575-F1586, 2009. First published September 23, 2009; doi:10.1152/ajprenal.90762.2008.-Aquaporin 1 (AQP1) is the major water channel in the renal proximal tubule (PT) and thin descending limb of Henle, but its regulation remains elusive. Here, we investigated the effect of ANG II, a key mediator of body water homeostasis, on AQP1 expression in immortalized rat proximal tubule cells (IRPTC) and rat kidney. Real-time PCR on IRPTC exposed to ANG II for 12 h revealed a biphasic effect AQP1 mRNA increased dose dependently in response to 10(-12) to 10(-8) M ANG II but decreased by 50% with 10(-7) M ANG II. the twofold increase of AQP1 mRNA in the presence of 10(-8) M ANG II was abolished by the AT(1) receptor blocker losartan. Hypertonicity due to either NaCl or mannitol also upregulated AQP1 mRNA by three- and twofold, respectively. Immunocytochemistry and Western blotting revealed a two- to threefold increase in AQP1 protein expression in IRPTC exposed concomitantly to ANG II (10(-8)M) and hypertonic medium (either NaCl or mannitol), indicating that these stimuli were not additive. Three-dimensional reconstruction of confocal images suggested that AQP1 expression was increased by ANG II in both the apical and basolateral poles of IRPTC. in vivo studies showed that short-term ANG II infusion had a diuretic effect, while this effect was attenuated after several days of ANG II infusion. After 10 days, we observed a twofold increase in AQP1 expression in the PT and thin descending limb of Henle of ANG II-infused rats that was abolished when rats were treated with the selective AT(1)-receptor antagonist olmesartan. Thus ANG II increases AQP1 expression in vitro and in vivo via direct interaction with the AT(1) receptor, providing an important regulatory mechanism to link PT water reabsorption to body fluid homeostasis via the renin-angiotensin system.en
dc.description.affiliationHarvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Syst Biol,Program Membrane Biol,Nephrol Div, Boston, MA 02114 USA
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Nephrol, São Paulo, Brazil
dc.description.affiliationHarvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02114 USA
dc.description.affiliationTulane Univ, Hlth Sci Ctr, Dept Physiol & Hypertens, New Orleans, LA 70118 USA
dc.description.affiliationInst Med Res & Occupat Hlth, Zagreb 41000, Croatia
dc.description.affiliationMassachusetts Gen Hosp, Boston, MA 02114 USA
dc.description.affiliationGeorgetown Univ, Dept Pediat, Washington, DC 20057 USA
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Disciplina Nephrol, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipNational Heart, Lung, and Blood Institute
dc.description.sponsorshipNational Institute of Diabetes and Digestive and Kidney Diseases
dc.description.sponsorshipNational Kidney Foundation Investigator Award
dc.description.sponsorshipNational Sciences and Engineering Research Council
dc.description.sponsorshipBoston Area Diabetes and Endocrinology Research Center
dc.description.sponsorshipCenter for the Study of Inflammatory Bowel Disease
dc.description.sponsorshipIDNational Heart, Lung, and Blood Institute: HL-40210
dc.description.sponsorshipIDNational Heart, Lung, and Blood Institute: HL-48455
dc.description.sponsorshipIDNational Institute of Diabetes and Digestive and Kidney Diseases: PO1-DK-38452
dc.description.sponsorshipIDNational Institute of Diabetes and Digestive and Kidney Diseases: DK-38452
dc.description.sponsorshipIDBoston Area Diabetes and Endocrinology Research Center: DK-57521
dc.description.sponsorshipIDCenter for the Study of Inflammatory Bowel Disease: DK-43351
dc.format.extentF1575-F1586
dc.identifierhttp://dx.doi.org/10.1152/ajprenal.90762.2008
dc.identifier.citationAmerican Journal of Physiology-renal Physiology. Bethesda: Amer Physiological Soc, v. 297, n. 6, p. F1575-F1586, 2009.
dc.identifier.doi10.1152/ajprenal.90762.2008
dc.identifier.issn1931-857X
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/31965
dc.identifier.wosWOS:000273288100011
dc.language.isoeng
dc.publisherAmer Physiological Soc
dc.relation.ispartofAmerican Journal of Physiology-renal Physiology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectrenin angiotensin systemen
dc.subjectproximal tubuleen
dc.titleAngiotensin II and hypertonicity modulate proximal tubular aquaporin 1 expressionen
dc.typeinfo:eu-repo/semantics/article
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