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Tytuł pozycji:

Renal ischemia-reperfusion leads to hypertension and changes in proximal tubule Na + transport and renin-angiotensin-aldosterone system: Role of NADPH oxidase.

Tytuł:
Renal ischemia-reperfusion leads to hypertension and changes in proximal tubule Na transport and renin-angiotensin-aldosterone system: Role of NADPH oxidase.
Autorzy:
Lima NKS; Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil.
Farias WRA; Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil.
Cirilo MAS; Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil.
Oliveira AG; Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil.
Farias JS; Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil.
Aires RS; Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil.
Muzi-Filho H; Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; National Center for Structural Biology and Bioimaging/CENABIO, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Paixão ADO; Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil; National Center for Structural Biology and Bioimaging/CENABIO, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Vieira LD; Department of Physiology and Pharmacology, Federal University of Pernambuco, Recife, Brazil; National Center for Structural Biology and Bioimaging/CENABIO, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: .
Źródło:
Life sciences [Life Sci] 2021 Feb 01; Vol. 266, pp. 118879. Date of Electronic Publication: 2020 Dec 10.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
MeSH Terms:
Renin-Angiotensin System*
Acute Kidney Injury/*complications
Hypertension/*pathology
Kidney Tubules, Proximal/*pathology
NADPH Oxidases/*metabolism
Reperfusion Injury/*complications
Sodium/*metabolism
Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Aldosterone/metabolism ; Animals ; Hypertension/enzymology ; Hypertension/etiology ; Kidney Tubules, Proximal/metabolism ; Male ; Oxidative Stress ; Rats ; Rats, Wistar ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology
Contributed Indexing:
Keywords: Acute kidney injury; Hypertension; Ischemia-reperfusion; NADPH oxidase; Renin-angiotensin-aldosterone system
Substance Nomenclature:
4964P6T9RB (Aldosterone)
9NEZ333N27 (Sodium)
EC 1.6.3.- (NADPH Oxidases)
Entry Date(s):
Date Created: 20201214 Date Completed: 20210201 Latest Revision: 20210201
Update Code:
20240104
DOI:
10.1016/j.lfs.2020.118879
PMID:
33310030
Czasopismo naukowe
Acute renal injury (AKI) is a risk factor for the development of hypertension, which involves oxidative stress, changes in Na + handling, and the intrarenal renin-angiotensin-aldosterone system (RAAS) as underlying mechanisms. We investigated in rats whether renal ischemia-reperfusion (IR) leads to changes in the proximal tubule ATP-dependent Na + transport and the intrarenal content of RAAS components, as well as the role of NADPH oxidase. Rats weighing 300-350 g were submitted to AKI by bilateral IR (n = 25). After IR injury, the animals were followed up for 4 weeks. One part (n = 7) received daily treatment with the NADPH oxidase inhibitor apocynin (100 mg/kg, drinking water), while another part (n = 9) received apocynin 24 h before and after IR. One group was submitted to sham surgery (n = 8). Four weeks after IR, the rats presented elevated systolic blood pressure, as well as increased lipid peroxidation, NADPH oxidase activity, (Na + +K + )ATPase activity, and upregulation of type 1 angiotensin II receptor in the renal cortex. On the other hand, there was a decrease in Na + -ATPase activity and downregulation of the isoforms 1 and 2 of the angiotensin-converting enzyme, type 2 angiotensin II receptor, and of the α and ε isoforms of protein kinase C. Most of these alterations was prevented by both apocynin treatment protocols. Thus, we conclude that AKI-induced by IR may induce changes in proximal tubule ATPases and RAAS components compatible with renal Na + retention and hypertension. These data also indicate that the NADPH oxidase represents a key factor in the origin of these alterations.
(Copyright © 2020 Elsevier Inc. All rights reserved.)

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