Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Ferreira, Anderson J.; Santos, Robson Augusto Souza; Almeida, Alvair P.

doi:10.1590/s0100-879x2002000900009

Cited by 82 publications

(75 citation statements)

References 37 publications

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“…5 A large body of evidence has accumulated over the past two decades to support the notion that angiotensin II, through its AT1 receptor, mediates myocardial interstitial fibrosis and cardiomyocyte hypertrophy, 9,10 but it does not directly stimulate cardiomyocytes growth and fibrosis in the adult myocardium, but does so indirectly by inducing the expression of TGF-b, which then acts locally through the auto/paracrine mechanism. 11,12 TGF-b is a locally generated cytokine that has been implicated as a major contributor to tissue fibrosis in various organ systems. 13 Antagonists of the RAS, such as ACE inhibitors and angiotensin-receptor blockers, attenuate the fibrotic changes and matrix deposition mediated by TGF-b.…”

Section: Angiotensin (1à7) Prevent Heart Dysfunction and Left Ventricmentioning

confidence: 99%

“…11 It has also been found that Ang (1-7) have a cardioprotective effect in the rat. Ang (1-7) decrease the incidence and duration of ischemia/reperfusion arrhythmias 12 and improve post-ischemic function in the isolated rat heart. 13 Angs (1-7) are also effective in preventing heart failure after myocardial ischemia, induced by left coronary artery ligation.…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

et al. 2009

Hypertens Res

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The renin-angiotensin system (RAS) plays a critical role in chronic renal failure associated with heart failure. In the past few years, angiotensin (Ang) (1-7) have been reported to counteract the effects of angiotensin II (Ang II) and were even considered as a new therapeutical target in RAS. The purposes of this study were to examine whether the Ang (1-7) improves the heart function and remodeling of the left ventricle (LV) in mice with 5/6 nephrectomy (NC). We used a 5/6 nephrectomy to induce significant renal dysfunction in wildtype mice (WT). Twelve weeks after NC, WT showed high blood pressure, significant leftventricular dilation and dysfunction, which were accompanied by cardiomyocyte hypertrophy, diffuse interstitial fibrosis and oxidative damage of cardiomyocytes. Exogenous Ang (1-7) injection improved the heart function and remodeling of LV in mice with 5/6 NC accompanied by a reduction in cardiac interstitial fibrosis, inflammatory cytokine expression and oxidative damage levels of cardiomyocytes, decrease in the profibrotic signaling molecule transforming growth factor (TGF)-b and increase in the collagen degradation signaling molecule matrix metalloproteinase (MMP)-2, -9. However, these beneficial effects did not occur in hydralazine-treated mice. These findings suggest that (1) Exogenous Ang (1-7) injection improve the heart function and remodeling of LV in mice with 5/6 NC. (2) These beneficial effects are independent of its anti-blood pressure effect.

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Section: Angiotensin (1à7) Prevent Heart Dysfunction and Left Ventricmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

et al. 2009

Hypertens Res

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“…1] by our laboratory in 1988 (Schiavone et al 1988) and the cloning of ACE2 in 2000 (Donoghue et al 2000;Tipuis et al 2000) have led to a new perception of the intrinsic mechanisms through which the RAS regulates homeostasis. Ang-(1-7) is a downstream heptapeptide product of the system that can regulate blood pressure (Benter et al 1995b;Ferrario et al 2005), cardiac function (Ferreira et al 2002;Loot et al 2002;De Mello et al 2004), and cell growth (Tallant et al 2005).…”

Section: Angiotensin-(1-7) 163mentioning

confidence: 99%

Angiotensin‐(1‐7): Pharmacology and New Perspectives in Cardiovascular Treatments

Trask

Ferrario

2007

Cardiovascular Drug Reviews

101

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Many advances have been made in the cardiovascular field in the last several decades. Among them is the progress completed to date on the heptapeptide member of the reninangiotensin system (RAS), angiotensin-(1-7) [Ang-(1-7)]. The peptide's beneficial actions against pathophysiological processes, such as cardiac arrhythmia, heart failure, hypertension, renal disease, preeclampsia, and even cancer are continuously being uncovered. This review encompasses the pharmacology of Ang-(1-7) and expounds upon the peptide's potential as a therapeutic agent against pathological processes both within and outside the cardiovascular continuum.

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“…7 In addition to its vascular effects, it was shown that Ang-(1-7) also has beneficial effects on cardiac function. [9][10][11] Moreover, it opposes the growth-stimulating effects of Ang II in vascular smooth muscle cells 12 and cardiomyocytes. 13 Ang-(1-7) also demonstrates effects on renal function by participating in the control of water and electrolyte homeostasis.…”

Section: Introductionmentioning

confidence: 99%

Hemodynamic effects of vasorelaxant compounds in mice lacking one, two or all three angiotensin II receptors

et al. 2012

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The renin-angiotensin system (RAS) has a vital role in regulating the cardiovascular system. The primary effector of the RAS is the octapeptide angiotensin (Ang) II, a potent regulator of blood pressure and water homeostasis. Ang II mediates its functions through the stimulation of two distinct receptors, AT 1 (two subtypes in rodents (AT 1a and AT 1b )) and AT 2 . It was shown that in addition to Ang II, shorter fragments of Ang are also biologically active. Ang-(1-7) came into focus because it opposes many of the detrimental effects of Ang II. However, it is still controversial whether Ang II receptors are involved in Ang-(1-7)-mediated signaling. To characterize the impacts of Ang II receptors on Ang-(1-7)-stimulated vascular relaxation, the effects of acute infusion of the three vasorelaxant compounds, that is, Ang-(1-7), bradykinin (BK) and acetylcholine (ACh), on heart rate (HR) and mean arterial pressure (MAP) were investigated in mice deficient for one, two or all three Ang II receptors. Ang-(1-7) and BK reduced MAP in wild-type, AT 1a /AT 1b -deficient and AT 2 -deficient mice. Although the change in absolute MAP values in the hypotensive triple knockouts (KO) could not be further reduced by both peptides, the percent change in MAP was comparable between the triple KO and wild-type mice. Both peptides did not alter the HR in all four genotypes. ACh significantly reduced absolute MAP values in all four genotypes with a similar percentage of reduction. In contrast to Ang-(1-7) and BK, ACh significantly reduced HR without genotypic differences. Our results generate proof that Ang-(1-7)-induced effects on MAP are mediated by a receptor that is independent of AT 1 and AT 2 .

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Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

Cited by 82 publications

References 37 publications

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

Angiotensin‐(1‐7): Pharmacology and New Perspectives in Cardiovascular Treatments

Hemodynamic effects of vasorelaxant compounds in mice lacking one, two or all three angiotensin II receptors

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