Angiotensin II and the Heart

Mello, Walmor C. De; Danser, A.H. Jan

doi:10.1161/01.hyp.35.6.1183

Cited by 245 publications

(82 citation statements)

References 111 publications

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“…Additionally, ACE inhibitors attenuate not only the production of Ang II at a systemic and tissue level, but they also allow the accumulation of bradykinin because they inhibit its degradation [20,21,22,23]. Animal studies have shown that the inhibition of bradykinin degradation contributes more to the reduction in blood pressure than the inhibition of Ang II formation by ACE inhibitors [24,25,26,27].…”

Section: Discussionmentioning

confidence: 99%

Comparative Effects of a Novel Angiotensin-Converting Enzyme Inhibitor versus Captopril on Plasma Angiotensins after Myocardial Infarction

Flores-Monroy

Ferrario²,

Valencia-Hernández³

et al. 2014

Pharmacology

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The compound 4-tert-butyl-2,6-bis(thiomorpholin-4-ylmethyl)phenol (TBTIF) has molecular characteristics similar to angiotensin-converting enzyme (ACE) inhibitors of the sulfhydryl subclass. To assess its value as a new therapeutic agent, we performed a comparative analysis of the effect of TBTIF versus captopril on the circulating levels of angiotensin (Ang) peptides and bradykinin as well as ACE and ACE2 expression after myocardial infarction. Male Wistar rats were divided into four groups: (1) sham-operated rats; (2) rats subjected to 48 h of coronary artery ligation; (3) rats administered captopril (1 mg/kg, i.m.), and (4) a similar group of rats given TBTIF (1 mg/kg, i.m.). Both drugs were administered 30 min before coronary artery ligation and again 24 h later. Acute myocardial infarction lowered both systolic and left ventricular systolic blood pressures compared to the sham group and increased plasma levels of Ang I, Ang II, Ang(1-7) and Ang(1-12). Administration of either captopril or TBTIF reversed the increases in plasma angiotensins. Interestingly, the levels of plasma Ang(1-7) achieved by administration of TBTIF reached values higher than those recorded with captopril. Both agents reversed the decreases in plasma concentrations of bradykinin; in addition, TBTIF upregulated ACE expression, while both agents suppressed the ACE2 upregulation induced by myocardial infarction. These results demonstrate a beneficial effect of the novel compound TBTIF in suppressing the acute surge in the circulating renin-angiotensin system activity induced by myocardial infarction. The greater effects of this compound in augmenting plasma Ang(1-7) concentrations may be highly significant as drugs which augment the concentration of this heptapeptide will exert cardioprotective actions in part by suppressing the hypertrophic and profibrotic actions of Ang II.

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Section: Discussionmentioning

confidence: 99%

Comparative Effects of a Novel Angiotensin-Converting Enzyme Inhibitor versus Captopril on Plasma Angiotensins after Myocardial Infarction

Flores-Monroy

Ferrario²,

Valencia-Hernández³

et al. 2014

Pharmacology

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“…This suggests that at least in some species, the heart is a site of extrarenal renin production. Other authors have suggested that, whereas renin is not synthesized in the heart under physiological conditions, renin gene expression may be turned on in pathophysiological situations (147). It is interesting to note in this context that an additional truncated renin mRNA has been described in heart tissue which lacks the prefragment of preprorenin and results in the formation of a truncated prorenin protein termed exon 1A renin (103,541).…”

Section: Reninmentioning

confidence: 95%

Physiology of Local Renin-Angiotensin Systems

Paul

Mehr²,

Kreutz³

2006

Physiological Reviews

1,503

1,371

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Since the first identification of renin by Tigerstedt and Bergmann in 1898, the renin-angiotensin system (RAS) has been extensively studied. The current view of the system is characterized by an increased complexity, as evidenced by the discovery of new functional components and pathways of the RAS. In recent years, the pathophysiological implications of the system have been the main focus of attention, and inhibitors of the RAS such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin (ANG) II receptor blockers have become important clinical tools in the treatment of cardiovascular and renal diseases such as hypertension, heart failure, and diabetic nephropathy. Nevertheless, the tissue RAS also plays an important role in mediating diverse physiological functions. These focus not only on the classical actions of ANG on the cardiovascular system, namely, the maintenance of cardiovascular homeostasis, but also on other functions. Recently, the research efforts studying these noncardiovascular effects of the RAS have intensified, and a large body of data are now available to support the existence of numerous organ-based RAS exerting diverse physiological effects. ANG II has direct effects at the cellular level and can influence, for example, cell growth and differentiation, but also may play a role as a mediator of apoptosis. These universal paracrine and autocrine actions may be important in many organ systems and can mediate important physiological stimuli. Transgenic overexpression and knock-out strategies of RAS genes in animals have also shown a central functional role of the RAS in prenatal development. Taken together, these findings may become increasingly important in the study of organ physiology but also for a fresh look at the implications of these findings for organ pathophysiology.

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“…In turn, the terminal two amino acids of angiotensin I are cleaved by angiotensin-converting enzyme (ACE) to yield Ang II, the effector molecule of the renin-angiotensin system (RAS). The presence of a local, as distinct from a systemic RAS, has been established in several organs including the heart, adrenal gland, thymus and ovary [7, 8, 9, 10, 11, 12]. This is also true for the eye, following the identification of RAS components including angiotensinogen, renin and ACE within the eyes of humans, rats and other mammals [13, 14, 15, 16].…”

Section: The Ocular Renin-angiotensin System: Characterization and Nomentioning

confidence: 99%

The Interaction between the Renin-Angiotensin System and Vascular Endothelial Growth Factor in the Pathogenesis of Retinal Neovascularization in Diabetes

Wilkinson-Berka

Kelly²,

Gilbert³

2001

J Vasc Res

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Despite the use of laser photocoagulation and knowledge of the beneficial effects of good glycaemic control, visual loss due to diabetic retinopathy remains the commonest cause of blindness in the working population. This visual loss is principally the result of proliferative diabetic retinopathy and macular oedema. The processes by which diabetes mellitus results in retinopathy are incompletely understood, but recent evidence has suggested a pathogenetic role for the renin-angiotensin system (RAS) and vascular endothelial growth factor (VEGF) in the eye in response to chronic hyperglycaemia. This review will explore evidence of a local RAS in the eye, the involvement of VEGF in diabetic retinopathy and the interaction between the RAS and VEGF in the pathogenesis of retinal neovascularization.

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Angiotensin II and the Heart

Cited by 245 publications

References 111 publications

Comparative Effects of a Novel Angiotensin-Converting Enzyme Inhibitor versus Captopril on Plasma Angiotensins after Myocardial Infarction

Comparative Effects of a Novel Angiotensin-Converting Enzyme Inhibitor versus Captopril on Plasma Angiotensins after Myocardial Infarction

Physiology of Local Renin-Angiotensin Systems

The Interaction between the Renin-Angiotensin System and Vascular Endothelial Growth Factor in the Pathogenesis of Retinal Neovascularization in Diabetes

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