Key result
Interruption of angiotensin II activity with ACE inhibitors and ARBs reduces proinflammatory mediators and oxidative stress, offering protective benefits independent of antihypertensive effects.
Why the study?
Does angiotensin II interruption reduce proinflammatory mediators and oxidative stress in inflammatory models and patients with inflammatory diseases?
Does angiotensin II interruption reduce proinflammatory mediators and oxidative stress in inflammatory models and patients with inflammatory diseases?
Angiotensin II interruption with ACE inhibitors and ARBs exhibits potent anti-inflammatory properties independent of blood pressure reduction, suggesting potential utility in inflammatory diseases.
Angiotensin II, the major effector molecule produced from the renin-angiotensin-aldosterone axis, is a vasoconstrictor contributing to hypertension. Evidence indicates, however, that angiotensin II also is a potent proinflammatory mediator with growth and remodeling effects. In vitro and in vivo studies have shown that angiotensin II blockade significantly reduces concentrations of proinflammatory mediators and oxidative stress products in numerous inflammatory models. Interruption of angiotensin II activity with angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers has been beneficial for patients with inflammatory diseases. Much of this benefit occurs independent of the antihypertensive effect of angiotensin II interruption, suggesting a distinctive protective mechanism. Angiotensin II receptor blockers may represent a novel class of antiinflammatory drugs with indications far beyond cardiovascular diseases.
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Dagenais et al. (2005) conducted a review in Inflammatory diseases. Angiotensin II interruption (ACE inhibitors and ARBs) was evaluated. Interruption of angiotensin II activity with ACE inhibitors and ARBs reduces proinflammatory mediators and oxidative stress, offering protective benefits independent of antihypertensive effects.
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