ArticleBritish journal of pharmacology2012
Role of H(2)O(2) in hypertension, renin-angiotensin system activation and renal medullary disfunction caused by angiotensin II.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 44 citations in OpenAlex.
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- Fumarate and its downstream signalling pathways in the cardiorenal system: Recent insights and novel expositions in the etiology of hypertension.European journal of pharmacology · 2023Review
- Indoxyl-Sulfate-Induced Redox Imbalance in Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Hydrogen peroxide (HScientific reports · 2021Article
- Renal Hydrogen Peroxide Production Prevents Salt-Sensitive Hypertension.Journal of the American Heart Association · 2020Article
- The Mechanism of Action of Ethoxidol on Oxidative Stress Indices in Heart Failure and Hypotension.Sovremennye tekhnologii v meditsine · 2020Article
- Apocynin and catalase prevent hypertension and kidney injury in Cyclosporine A-induced nephrotoxicity in rats.PloS one · 2020Article
- Angiotensin II-induced hypertension and cardiac hypertrophy are differentially mediated by TLR3- and TLR4-dependent pathways.American journal of physiology. Heart and circulatory physiology · 2019Article
- Antihypertensive effects of the hydro-ethanol extract of Senecio serratuloides DC in rats.BMC complementary and alternative medicine · 2019Article
- Prorenin receptor (PRR)-mediated NADPH oxidase (Nox) signaling regulates VEGF synthesis under hyperglycemic condition in ARPE-19 cells.Journal of receptor and signal transduction research · 2017Article
- Longer duration of obesity is associated with a reduction in urinary angiotensinogen in prepubertal children.Pediatric nephrology (Berlin, Germany) · 2017Article
- Oxidant Mechanisms in Renal Injury and Disease.Antioxidants & redox signaling · 2016Review
- Activation of adenosine receptors improves renal antioxidant status in diabetic Wistar but not SHR rats.Upsala journal of medical sciences · 2014Article
- Contribution of endogenously produced reactive oxygen species to the activation of podocyte NLRP3 inflammasomes in hyperhomocysteinemia.Free radical biology & medicine · 2014Article
- Oxidative stress in hypertension: role of the kidney.Antioxidants & redox signaling · 2014Review
- Maintenance of hypertensive hemodynamics does not depend on ROS in established experimental chronic kidney disease.PloS one · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
background and purposeActivation of the intrarenal renin-angiotensin system (RAS) and increased renal medullary hydrogen peroxide (H(2) O(2) ) contribute to hypertension. We examined whether H(2) O(2) mediated hypertension and intrarenal RAS activation induced by angiotensin II (Ang II). EXPERIMENTAL APPROACH: Ang II (200 ng·kg(-1) ·min(-1) ) or saline were infused in Sprague Dawley rats from day 0 to day 14. Polyethylene glycol (PEG)-catalase (10 000 U·kg(-1) ·day(-1) ) was given to Ang II-treated rats, from day 7 to day 14. Systolic blood pressure was measured throughout the study. H(2) O(2) , angiotensin AT(1) receptor and Nox4 expression and nuclear factor-κB (NF-κB) activation were evaluated in the kidney. Plasma and urinary H(2) O(2) and angiotensinogen were also measured. KEY
resultsAng II increased H(2) O(2) , AT(1) receptor and Nox4 expression and NF-κB activation in the renal medulla, but not in the cortex. Ang II raised plasma and urinary H(2) O(2) levels, increased urinary angiotensinogen but reduced plasma angiotensinogen. PEG-catalase had a short-term antihypertensive effect and transiently suppressed urinary angiotensinogen. PEG-catalase decreased renal medullary expression of AT(1) receptors and Nox4 in Ang II-infused rats. Renal medullary NF-κB activation was correlated with local H(2) O(2) levels and urinary angiotensinogen excretion. Loss of antihypertensive efficacy was associated with an eightfold increase of plasma angiotensinogen. CONCLUSIONS AND IMPLICATIONS: The renal medulla is a major target for Ang II-induced redox dysfunction. H(2) O(2) appears to be the key mediator enhancing intrarenal RAS activation and decreasing systemic RAS activity. The specific control of renal medullary H(2) O(2) levels may provide future grounds for the treatment of hypertension.
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