It is now well established that the activation of the renin-angiotensin system (RAS) is involved in the onset and progression of cardiovascular and renal diseases, and that its main effector, angiotensin II (Ang II) has major pro-inflammatory activity that induces the expression of cytokines, chemokines, adhesion molecules, growth factors and reactive oxygen species. By means of these actions, Ang II induces vascular inflammation, endothelial dysfunction and fibrosis, and participates in destabilizing atherosclerotic plaque and establishing chronic kidney diseases. Blocking the RAS by inhibiting Ang II generation or blocking angiotensin receptors reduces the morbidity and mortality associated with cardiovascular and renal disease beyond the levels due to the lowering of blood pressure, and these benefits are at least partially due to the reduction/prevention of both local and systemic inflammatory processes. The aim of this review is to describe the role of the RAS (and particularly Ang II) in initiating and maintaining these processes, and to summarize experimental and clinical evidence supporting the role of drugs acting on the RAS in preventing or modulating inflammation.

Anti-inflammatory properties of drugs acting on the renin-angiotensin system / L. Sironi, E. Nobili, A. Gianella, P. Gelosa, E. Tremoli.. - In: DRUGS OF TODAY. - ISSN 1699-3993. - 41:9(2005), pp. 609-622. [10.1358/dot.2005.41.9.899613]

Anti-inflammatory properties of drugs acting on the renin-angiotensin system

L. Sironi
Primo
;
E. Nobili
Secondo
;
P. Gelosa
Penultimo
;
E. Tremoli
Ultimo
2005

Abstract

It is now well established that the activation of the renin-angiotensin system (RAS) is involved in the onset and progression of cardiovascular and renal diseases, and that its main effector, angiotensin II (Ang II) has major pro-inflammatory activity that induces the expression of cytokines, chemokines, adhesion molecules, growth factors and reactive oxygen species. By means of these actions, Ang II induces vascular inflammation, endothelial dysfunction and fibrosis, and participates in destabilizing atherosclerotic plaque and establishing chronic kidney diseases. Blocking the RAS by inhibiting Ang II generation or blocking angiotensin receptors reduces the morbidity and mortality associated with cardiovascular and renal disease beyond the levels due to the lowering of blood pressure, and these benefits are at least partially due to the reduction/prevention of both local and systemic inflammatory processes. The aim of this review is to describe the role of the RAS (and particularly Ang II) in initiating and maintaining these processes, and to summarize experimental and clinical evidence supporting the role of drugs acting on the RAS in preventing or modulating inflammation.
antiinflammatory activity; clinical trial; coronary artery disease; diabetic nephropathy; enzyme inhibition; gene expression; human; hypertension; inflammation; kidney disease; kidney failure; microalbuminuria; nonhuman; pathophysiology; protein function; renin angiotensin aldosterone system; review; vascular disease; 2 ethyl 5,7 dimethyl 3 [4 [2 (2h tetrazol 5 yl)phenyl]benzyl]imidazo[4,5 b]pyridine; angiotensin 1 receptor antagonist; angiotensin 2 receptor antagonist; antiinflammatory agent; atenolol; benazepril; candesartan hexetil; captopril; dipeptidyl carboxypeptidase inhibitor; enalapril; fosinopril; hydrochlorothiazide; irbesartan; lisinopril; losartan; olmesartan; quinapril; ramipril; telmisartan; valsartan; l 158809
Settore BIO/14 - Farmacologia
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/9564
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