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

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 c...

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Published in:Life sciences (1973) 2021-02, Vol.266, p.118879-118879, Article 118879
Main Authors: Lima, Natália K.S., Farias, Wilka R.A., Cirilo, Marry A.S., Oliveira, Angélica G., Farias, Juliane S., Aires, Regina S., Muzi-Filho, Humberto, Paixão, Ana D.O., Vieira, Leucio D.
Format: Article
Language:English
Subjects:
Acute kidney injury
Acute Kidney Injury - complications
Acute Kidney Injury - metabolism
Acute Kidney Injury - pathology
Aldosterone
Aldosterone - metabolism
Angiotensin
Angiotensin II
Animals
Blood pressure
Drinking water
Hypertension
Hypertension - enzymology
Hypertension - etiology
Hypertension - pathology
Ischemia
Ischemia-reperfusion
Isoforms
Kidney Tubules, Proximal - metabolism
Kidney Tubules, Proximal - pathology
Kinases
Lipid peroxidation
Lipids
Male
Na+/K+-exchanging ATPase
NAD(P)H oxidase
NADPH oxidase
NADPH Oxidases - metabolism
Oxidase
Oxidative Stress
Peptidyl-dipeptidase A
Peroxidation
Protein kinase C
Rats
Rats, Wistar
Receptors
Renal cortex
Renin
Renin-Angiotensin System
Renin-angiotensin-aldosterone system
Reperfusion
Reperfusion Injury - complications
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
Risk analysis
Risk factors
Sodium
Sodium - metabolism
Surgery
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Summary: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.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2020.118879