Advances in the Renin Angiotensin System

Ferrario, Carlos M.; Ahmad, Sarfaraz; Joyner, JaNae; Varagić, Jasmina

doi:10.1016/s1054-3589(10)59007-0

Cited by 54 publications

(32 citation statements)

References 291 publications

(402 reference statements)

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“…Ang-(1-7) accumulation after ACE inhibition can be due to an increase in AngI and/or decrease in its own inactivation, because ACE is an important route for the metabolism of Ang-(1-7) [46]. Previous studies from our group showed that the baroreflex improvement induced by ACE inhibition in hypertensive rats was mediated by the action of Ang- (1)(2)(3)(4)(5)(6)(7) in the brain [47,48]. We tested for this possibility and observed that the selective Mas receptor antagonist, A779, reversed the anxiolytic-like effect induced by enalapril treatment.…”

Section: Discussionmentioning

confidence: 92%

“…However, ACE inhibition not only interferes with Ang II formation but also increases the concentration of Ang- (1)(2)(3)(4)(5)(6)(7). This effect was demonstrated in the circulation of spontaneous hypertensive rats [23] and humans [22].…”

Section: Discussionmentioning

confidence: 96%

“…In the long term, the RAS operates through the balance of two major pathways: the angiotensin-converting enzyme (ACE)/angiotensin II (AngII)/AT 1 -receptor, the hypertensive and proliferative pathway; and the ACE2/angiotensin- (1)(2)(3)(4)(5)(6)(7) [Ang-(1-7)]/Mas receptor, the hypotensive and anti-proliferative pathway [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…Ang-(1-7) has multiple actions, most of which counteract those described for AngII [2,3]. Its effects occur mainly through activation of the G-protein-coupled receptor Mas [4], which is expressed in different tissues, including the brain [5,6].…”

Section: Introductionmentioning

confidence: 99%

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Anxiolytic- and antidepressant-like effects of angiotensin-(1–7) in hypertensive transgenic (mRen2)27 rats

et al. 2016

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Angiotensin-(1-7) [Ang-(1-7)], a counter-regulatory peptide of the renin-angiotensin system (RAS) exerts its effects through the G-protein-coupled receptor Mas, which is expressed in different tissues, including the brain. Ang-(1-7) has a broad range of effects beyond the well-described cardiovascular and renal actions, including the modulation of emotional and behavioural responses. In the present study we tested the hypothesis that Ang-(1-7) could attenuate the anxiety- and depression-like behaviours observed in transgenic hypertensive (mRen2)27 rats (TGRs). We also hypothesized that Ang-(1-7) could be involved in the anxiolytic-like effect induced by ACE (angiotensin-converting enzyme) treatment in these hypertensive rats. Therefore, TGRs and Sprague-Dawley rats were subjected to the Elevated Plus Maze (EPM) test, Forced Swimming Test (FST) and Novelty Suppressed Feeding (NSF). TGRs presented a decreased percentage of entries in the open arms of the EPM test, a phenotype reversed by systemic treatment with enalapril or intracerebroventricular infusion of Ang-(1-7). It is interesting that pre-treatment with A779, a selective Mas receptor antagonist, prevented the anxiolytic-like effect induced by the ACE inhibitor. In the NSF test, TGRs showed increased latency to eating, an indicative of a higher aversion in response to a new environment. These animals also showed increased immobility in the FST. Again, Ang-(1-7) reversed this phenotype. Thus, our data showed that Ang-(1-7) can modulate anxiety- and depression-like behaviours in TGRs and warrant further investigation as a new therapy for certain psychiatric disorders.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Anxiolytic- and antidepressant-like effects of angiotensin-(1–7) in hypertensive transgenic (mRen2)27 rats

et al. 2016

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“…During the last 25 years knowledge of the biochemical physiology of the circulating and tissue renin angiotensin system has grown exponentially through the discovery and characterization of the vasodilator and anti-proliferative actions of angiotensin-(1-7) [Ang-(1-7)] [1], the characterization of angiotensin converting enzyme 2 (ACE2) as an Ang-(1-7)-forming enzyme from angiotensin II (Ang II) [2–4], and the demonstration of the mas receptor as the endogenous binding protein for Ang-(1-7) [5]. On the 25 th anniversary of the publication of the first report describing the actions of Ang-(1-7) [6], the science presented at the XI International Symposium on Vasoactive Peptides (May 2–4, 2013, Belo Horizonte, Brazil) attested to the impressive progress achieved in deciphering the complexity of the biochemical and physiological processes by which the renin angiotensin system contributes to organ and cell homeostasis.…”

Section: Introduction –The Yesteryears–mentioning

confidence: 99%

An evolving story of angiotensin-II-forming pathways in rodents and humans

et al. 2013

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Lessons learned from the characterization of the biological roles of angiotensin-(1-7) in opposing the vasoconstrictor, proliferative, and prothrombotic actions of angiotensin II created an underpinning for a more comprehensive exploration of the multiple pathways by which the blood and tissues renin angiotensin system regulates homeostasis and its altered state in disease processes. This review summarizes the progress that has been made in the novel exploration of intermediate shorter forms of angiotensinogen through the characterization of the expression and functions of the dodecapeptide angiotensin-(1-12) in the cardiac production of angiotensin II. The studies reveal significant differences in humans versus rodents regarding the enzymatic pathway by which angiotensin-(1-12) undergoes metabolism. Highlights of the research include the demonstration of chymase-direct formation of angiotensin II from angiotensin-(1-12) in human left atrial myocytes and left ventricular tissue, the presence of robust expression of angiotensin-(1-12) and chymase in the atrial appendage of subjects with resistant atrial fibrillation, and the preliminary observation of significantly higher angiotensin-(1-12) expression in human left atrial appendages.

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