Alternate Angiotensin II-Forming Pathways and Their Importance in Physiological or Physiopathological Conditions

Resende, Micheline; Mill, José Geraldo

doi:10.1590/s0066-782x2002000400012

Cited by 21 publications

(16 citation statements)

References 61 publications

(61 reference statements)

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“…The cardiac RAAS is activated under several pathophysiological conditions, including MI and HF of different etiologies (27,28). Angiotensinogen is produced in infarcted hearts mainly by macrophages and fibroblasts, and ACE is extensively synthesized in endothelial cells and macrophages (29).…”

Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

Remodeling in the ischemic heart: the stepwise progression for heart

Mill¹,

Stefanon

Santos

et al. 2011

Braz J Med Biol Res

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Coronary artery disease is the leading cause of death in the developed world and in developing countries. Acute mortality from acute myocardial infarction (MI) has decreased in the last decades. However, the incidence of heart failure (HF) in patients with healed infarcted areas is increasing. Therefore, HF prevention is a major challenge to the health system in order to reduce healthcare costs and to provide a better quality of life. Animal models of ischemia and infarction have been essential in providing precise information regarding cardiac remodeling. Several of these changes are maladaptive, and they progressively lead to ventricular dilatation and predispose to the development of arrhythmias, HF and death. These events depend on cell death due to necrosis and apoptosis and on activation of the inflammatory response soon after MI. Systemic and local neurohumoral activation has also been associated with maladaptive cardiac remodeling, predisposing to HF. In this review, we provide a timely description of the cardiovascular alterations that occur after MI at the cellular, neurohumoral and electrical level and discuss the repercussions of these alterations on electrical, mechanical and structural dysfunction of the heart. We also identify several areas where insufficient knowledge limits the adoption of better strategies to prevent HF development in chronically infarcted individuals.

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Section: The Cardiac Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

Remodeling in the ischemic heart: the stepwise progression for heart

Mill¹,

Stefanon

Santos

et al. 2011

Braz J Med Biol Res

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“…Although the importance of these alternative pathways is still controversial, some researchers recognize that chymase is the major route of angiotensin II synthesis in tissues and may be more important in the pathogenesis of cardiovascular disease than previously thought. 90 Thus, ACE inhibitor therapy may only partially inhibit angiotensin II activity, whereas ARB treatment prevents its activity without regard to its origin.…”

Section: Angiotensin-converting Enzyme Inhibitors and Angiotensin II mentioning

confidence: 99%

Protective Effects of Angiotensin II Interruption: Evidence for Antiinflammatory Actions

Dagenais

Jamali

2005

Pharmacotherapy

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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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“…Therefore, great caution must be exercised when extending to the human heart, data collected from other species 31 .…”

Section: Discussionmentioning

confidence: 99%

Enzima conversora de angiotensina no líquido pericárdico: estudo comparativo com a atividade sérica

Gomes¹,

Teodoro²,

Lopes³

et al. 2008

Arq. Bras. Cardiol.

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Alternate Angiotensin II-Forming Pathways and Their Importance in Physiological or Physiopathological Conditions

Abstract: Alternate angiotensin II-forming pathways Arq Bras Cardiol 2002; 78: 432-8.

Cited by 21 publications

References 61 publications

Remodeling in the ischemic heart: the stepwise progression for heart

Remodeling in the ischemic heart: the stepwise progression for heart

Protective Effects of Angiotensin II Interruption: Evidence for Antiinflammatory Actions

Enzima conversora de angiotensina no líquido pericárdico: estudo comparativo com a atividade sérica

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