Inflammation and angiotensin II

Suzuki, Yusuke; Ruíz-Ortega, Marta; Lorenzo, Óscar; Rupérez, Mónica; Esteban, Vanesa; Egido, Jesús

doi:10.1016/s1357-2725(02)00271-6

Cited by 635 publications

(502 citation statements)

References 187 publications

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“…Ang II, the main peptide hormone of RAS, is involved in several events during the inflammatory process (reviewed in Suzuki et al 27 ). Recently, increased Ang II concentration has been reported in animal tumor models 18 and some tumors are known to contain components of RAS, such as renin, ACE, or receptors for Ang II.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonist attenuate tumor growth via polarization of neutrophils toward an antitumor phenotype

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonist attenuate tumor growth via polarization of neutrophils toward an antitumor phenotype

et al. 2015

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“…Mesenteric artery VSMC growth in response to Ang II treatment appears to be regulated through an ERK 1/2-independent pathway. 31 Because different transcription factors, such as nuclear factor B, AP-1, and Sp1, can be activated by Ang II, 4,28,39 it is possible that chronic Ang II treatment may increase these transcription factors, which are implicated by ERK 1/2 gene expression regulation without altering ERK 1/2 activity. Moreover, increased activity of SHIP2 phosphatase in mesenteric arteries occurred after Ang II and rosiglitazone treatment.…”

Section: Discussionmentioning

confidence: 99%

Peroxisome Proliferator–Activated Receptor γ Regulates Angiotensin II–Stimulated Phosphatidylinositol 3-Kinase and Mitogen-Activated Protein Kinase in Blood Vessels In Vivo

et al. 2006

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Abstract-Angiotensin (Ang) II is implicated in hypertension, vascular remodeling, and insulin resistance. Peroxisome proliferator-activated receptor (PPAR) ␥ activators increase insulin sensitivity and improve Ang II-induced vascular remodeling. We evaluated the effects of the PPAR-␥ activator rosiglitazone on Ang II signaling in aorta and mesenteric arteries. Rats received Ang II by subcutaneous infusion and/or rosiglitazone per os for 7 days. Blood pressure rise in Ang II-infused rats was attenuated by rosiglitazone. Ang II significantly increased Ang II type 1 receptor expression in the mesenteric arteries (PϽ0.001), whereas that of the aorta was decreased (PϽ0.05), changes which were reversed by rosiglitazone. Akt activity was increased by Ang II and returned to basal levels under rosiglitazone in both vascular beds. However, Ang II-induced extracellular signal-regulated kinase 1/2 activity increased in aorta but not in mesenteric vessels (PϽ0.001), where 4E-binding protein 1 activity was significantly increased by Ang II and inhibited by PPAR-␥ activation. In response to Ang II, Src homology (SH) 2-containing inositol phosphatase 2 activity was increased (PϽ0.05) in both vascular beds. In conclusion, PPAR-␥ activator rosiglitazone attenuated Ang II-induced blood pressure elevation and intracellular signaling on aorta and mesenteric vessels. There was differential inhibition of Ang II type 1 receptor receptors/phosphatidylinositol 3-kinase/Akt and extracellular signal-regulated kinase 1/2 in both vessels. Effects of PPAR-␥ activators on these pathways could contribute to regression of vascular remodeling in models of hypertension and diabetes and, accordingly, in hypertensive diabetic patients.

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“…Chronic inflammation has been postulated to participate in the development of cardiovascular diseases, and recent data have shown that Ang II is an important proinflammatory mediator. 20 Thus, it is assumed that inflammation may play an important role in Ang II-induced cardiovascular alteration. Indeed, experimental studies have shown that Ang II infusion elicited the activation of NF-B in rat aortic and renal tissues, which was associated with inflammatory cell infiltration and tissue damage.…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 Inhibitors Attenuate Angiotensin II–Induced Oxidative Stress, Hypertension, and Cardiac Hypertrophy in Rats

Laplante

Champlain

2005

Hypertension

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Abstract-Angiotensin II is an important oxidative stress mediator. Our previous studies have indicated that the potent antioxidative properties of acetylsalicylic acid play an important role in its cardiovascular protective effects. There are some ongoing controversies concerning the use of selective cyclooxygenase-2 inhibitors in cardiovascular disease. The aim of this study was to determine whether the cyclooxygenase-2 selective inhibitors rofecoxib and nimesulide possess antioxidative and cardiovascular protective effects against angiotensin II. Chronic subcutaneous angiotensin II infusion increased cardiovascular but not colonic tissue superoxide production, heart/body weight ratio, and blood pressure. Moreover, angiotensin II selectively increased cardiac cyclooxygenase-2 but not cyclooxygenase-1 expression, which was totally prevented by acetylsalicylic acid treatment. Similar to acetylsalicylic acid, rofecoxib or nimesulide treatments significantly attenuated angiotensin II-induced oxidative stress, hypertension, and cardiac NAD(P)H oxidase subunit p47 phox expression. Rofecoxib also reduced cardiac hypertrophy. Treatment with nonselective anti-inflammatory drugs ibuprofen, indomethacin, or salicylic acid did not show any effect on angiotensin II-induced superoxide production, hypertension, or cardiac hypertrophy. Although acetylsalicylic acid and salicylic acid inhibited angiotensin II-induced nuclear factor B (NF-B) activation, nimesulide did not modify NF-B activation. In conclusion, cyclooxygenase-2 pathway is implicated in angiotensin II-induced oxidative stress and deleterious cardiovascular changes. Rofecoxib and nimesulide produced significant antioxidative effect by reducing NAD(P)H oxidase-dependent superoxide generation. These effects seem to be independent of NF-B inhibition.

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Inflammation and angiotensin II

Cited by 635 publications

References 187 publications

Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonist attenuate tumor growth via polarization of neutrophils toward an antitumor phenotype

Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonist attenuate tumor growth via polarization of neutrophils toward an antitumor phenotype

Peroxisome Proliferator–Activated Receptor γ Regulates Angiotensin II–Stimulated Phosphatidylinositol 3-Kinase and Mitogen-Activated Protein Kinase in Blood Vessels In Vivo

Cyclooxygenase-2 Inhibitors Attenuate Angiotensin II–Induced Oxidative Stress, Hypertension, and Cardiac Hypertrophy in Rats

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