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Angiotensin II type I receptor blockade suppresses glomerular renin-angiotensin system activation, oxidative stress, and progressive glomerular injury in rat anti-glomerular basement membrane glomerulonephritis.
Transl Res. 2011 Oct; 158(4):235-48.TR

Abstract

Excessive renin-angiotensin system (RAS) activation within the kidney induces not only renal oxidative stress but also renal scarring and dysfunction. This study examined the effects of an angiotensin II (Ang II) type I receptor (AT1R) blocker (ARB) on the progression of renal injury in rat anti-glomerular basement membrane glomerulonephritis (GN), with a particular focus on the participation of glomerular RAS activation in glomerular structural alterations, inflammation, and oxidative stress. Nephritic rats were divided into 2 groups and treated with vehicle or ARB until day 28. Treatment with ARB improved proteinuria significantly in nephritic rats. Vehicle-treated nephritic rats developed crescentic GN accompanied by marked macrophage infiltration and the enhanced expression of glomerular α-smooth muscle actin (α-SMA), angiotensinogen (AGT), Ang II, AT1R, and NADPH oxidase (Nox2) on days 7 and 28 of GN. ARB improved pathologic alterations such as crescent formation and glomerulosclerosis, and it had a significant inhibitory effect on the levels of these parameters on day 28 of GN. Enhanced superoxide production in nephritic glomeruli was decreased also by ARB. Moreover, Ang II and transforming growth factor beta (TGF-β) in the supernatant of cultured glomeruli was increased significantly in vehicle-treated nephritic rats whereas ARB inhibited the production of these compounds significantly on day 28. These results indicate that increased glomerular RAS activity and the resulting Ang II play important roles in progressive glomerular injury-the induction of oxidative stress and TGF-β expression, and they suggest that AT1R blockade attenuates proteinuria and progressive glomerular remodeling via the suppression of glomerular RAS activation in GN.

Authors+Show Affiliations

Department of Pediatrics, Institute of Health Bioscience, the University of Tokushima Graduate School, Tokushima, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21925120

Citation

Kinoshita, Yukiko, et al. "Angiotensin II Type I Receptor Blockade Suppresses Glomerular Renin-angiotensin System Activation, Oxidative Stress, and Progressive Glomerular Injury in Rat Anti-glomerular Basement Membrane Glomerulonephritis." Translational Research : the Journal of Laboratory and Clinical Medicine, vol. 158, no. 4, 2011, pp. 235-48.
Kinoshita Y, Kondo S, Urushihara M, et al. Angiotensin II type I receptor blockade suppresses glomerular renin-angiotensin system activation, oxidative stress, and progressive glomerular injury in rat anti-glomerular basement membrane glomerulonephritis. Transl Res. 2011;158(4):235-48.
Kinoshita, Y., Kondo, S., Urushihara, M., Suga, K., Matsuura, S., Takamatsu, M., Shimizu, M., Nishiyama, A., Kawachi, H., & Kagami, S. (2011). Angiotensin II type I receptor blockade suppresses glomerular renin-angiotensin system activation, oxidative stress, and progressive glomerular injury in rat anti-glomerular basement membrane glomerulonephritis. Translational Research : the Journal of Laboratory and Clinical Medicine, 158(4), 235-48. https://doi.org/10.1016/j.trsl.2011.05.003
Kinoshita Y, et al. Angiotensin II Type I Receptor Blockade Suppresses Glomerular Renin-angiotensin System Activation, Oxidative Stress, and Progressive Glomerular Injury in Rat Anti-glomerular Basement Membrane Glomerulonephritis. Transl Res. 2011;158(4):235-48. PubMed PMID: 21925120.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Angiotensin II type I receptor blockade suppresses glomerular renin-angiotensin system activation, oxidative stress, and progressive glomerular injury in rat anti-glomerular basement membrane glomerulonephritis. AU - Kinoshita,Yukiko, AU - Kondo,Shuji, AU - Urushihara,Maki, AU - Suga,Kenichi, AU - Matsuura,Sato, AU - Takamatsu,Masanori, AU - Shimizu,Maki, AU - Nishiyama,Akira, AU - Kawachi,Hiroshi, AU - Kagami,Shoji, Y1 - 2011/06/12/ PY - 2010/12/03/received PY - 2011/05/11/revised PY - 2011/05/13/accepted PY - 2011/9/20/entrez PY - 2011/9/20/pubmed PY - 2011/11/9/medline SP - 235 EP - 48 JF - Translational research : the journal of laboratory and clinical medicine JO - Transl Res VL - 158 IS - 4 N2 - Excessive renin-angiotensin system (RAS) activation within the kidney induces not only renal oxidative stress but also renal scarring and dysfunction. This study examined the effects of an angiotensin II (Ang II) type I receptor (AT1R) blocker (ARB) on the progression of renal injury in rat anti-glomerular basement membrane glomerulonephritis (GN), with a particular focus on the participation of glomerular RAS activation in glomerular structural alterations, inflammation, and oxidative stress. Nephritic rats were divided into 2 groups and treated with vehicle or ARB until day 28. Treatment with ARB improved proteinuria significantly in nephritic rats. Vehicle-treated nephritic rats developed crescentic GN accompanied by marked macrophage infiltration and the enhanced expression of glomerular α-smooth muscle actin (α-SMA), angiotensinogen (AGT), Ang II, AT1R, and NADPH oxidase (Nox2) on days 7 and 28 of GN. ARB improved pathologic alterations such as crescent formation and glomerulosclerosis, and it had a significant inhibitory effect on the levels of these parameters on day 28 of GN. Enhanced superoxide production in nephritic glomeruli was decreased also by ARB. Moreover, Ang II and transforming growth factor beta (TGF-β) in the supernatant of cultured glomeruli was increased significantly in vehicle-treated nephritic rats whereas ARB inhibited the production of these compounds significantly on day 28. These results indicate that increased glomerular RAS activity and the resulting Ang II play important roles in progressive glomerular injury-the induction of oxidative stress and TGF-β expression, and they suggest that AT1R blockade attenuates proteinuria and progressive glomerular remodeling via the suppression of glomerular RAS activation in GN. SN - 1878-1810 UR - https://www.unboundmedicine.com/medline/citation/21925120/Angiotensin_II_type_I_receptor_blockade_suppresses_glomerular_renin_angiotensin_system_activation_oxidative_stress_and_progressive_glomerular_injury_in_rat_anti_glomerular_basement_membrane_glomerulonephritis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1931-5244(11)00185-X DB - PRIME DP - Unbound Medicine ER -