Continuous angiotensin-(1–7) infusion improves myocardial calcium transient and calcium transient alternans in ischemia-induced cardiac dysfunction rats

Luo, Dong-Lei; Zhuang, Xiaodong; Luo, Can; Long, Ming; Chun-yu, Deng; Liao, Xinxue; Wang, Lichun

doi:10.1016/j.bbrc.2015.10.093

Cited by 4 publications

(4 citation statements)

References 27 publications

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“…As expected, interventions blocking Ang-(1-12)/chymase/Ang II as well as enhancing ACE2/Ang-(1-7) diminished aldosterone production [124,130]. It remains to be determined, however, which of the novel pharmacotherapies, shown to be effective in experimental heart failure including chymase inhibitors [131], recombinant human ACE2 [132][133][134], Ang-(1-7) [135], or combined angiotensin receptor antagonist and neprilysin inhibitor (ARNI) [104], are most effective in reducing the activity of aldosterone/mineralocorticoid receptor-dependent signaling. To exploit further these novel mechanisms pharmacotherapeutically, it is important to better understand the heterogeneity of local angiotensin pathways in various organs and their effects on aldosterone/mineralocorticoid receptor-dependent pathways.…”

Section: Resultsmentioning

confidence: 66%

Renin-Angiotensin-Aldosterone System in Heart Failure: Focus on Nonclassical Angiotensin Pathways as Novel Upstream Targets Regulating Aldosterone

Tyrankiewicz¹,

Kij²,

Mohaissen³

et al. 2019

Aldosterone-Mineralocorticoid Receptor - Cell Biology to Translational Medicine

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Aldosterone plays an important role in the regulation of blood pressure, body fluid, and electrolyte homeostasis. Overactivation of aldosterone/ mineralocorticoid receptor (MR) pathway leads to hypertension, atherosclerosis, vascular damage, heart failure, and chronic kidney disease and is involved in many other diseases associated with endothelial dysfunction, inflammation, fibrosis, and metabolic disorders. Aldosterone is a final product of the renin-angiotensin-aldosterone system (RAAS), and its production is activated by angiotensin II, while angiotensin-(1-7) negatively regulates angiotensin II-mediated aldosterone production and in some experimental models inhibits aldosterone-induced damage in target tissues. In fact, the aldosterone/mineralocorticoid receptor-dependent pathway is regulated upstream by at least two major axes of RAAS: classical axis (ACE/Ang II) and nonclassical axis (ACE2/Ang-(1-7)). The relative balance between these two axes determines aldosterone production and activity. To better understand the regulation of aldosterone activity in physiology and diseases, it is important to analyze the role of aldosterone/mineralocorticoid receptor-dependent pathways in the context of upstream angiotensin pathways as some of the recently described mechanisms of RAAS represent possible novel upstream targets to inhibit aldosterone/mineralocorticoid receptor-dependent responses. In this review, we highlight the complexity of angiotensin pathways focusing on their role in various tissues in heart failure, with particular emphasis on nonclassical pathways including protective ACE2/Ang-(1-7) axis and detrimental Ang-(1-12)/chymase/Ang II axis.

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Section: Resultsmentioning

confidence: 66%

Renin-Angiotensin-Aldosterone System in Heart Failure: Focus on Nonclassical Angiotensin Pathways as Novel Upstream Targets Regulating Aldosterone

Tyrankiewicz¹,

Kij²,

Mohaissen³

et al. 2019

Aldosterone-Mineralocorticoid Receptor - Cell Biology to Translational Medicine

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“…Cyclic angiotensin 1–7 reduced right ventricular (RV) systolic pressure, RV hypertrophy, and lung vascular remodeling [89]. Rats were subjected to permanent CAO [90]. Chronic infusion of angiotensin 1–7 increased LVDP [90].…”

Section: Angiotensin 1–7 Mitigated Adverse Remodeling Of the Heartmentioning

confidence: 99%

“…Rats were subjected to permanent CAO [90]. Chronic infusion of angiotensin 1–7 increased LVDP [90]. Chronic subcutaneous administration of angiotensin 1–7 (0.5 mg/kg/day) for 16 weeks improved contractility of the myocardium in type 2 diabetes (db/db) mice but did not alter cardiac hypertrophy [56].…”

Section: Angiotensin 1–7 Mitigated Adverse Remodeling Of the Heartmentioning

confidence: 99%

Angiotensin 1–7 increases cardiac tolerance to ischemia/reperfusion and mitigates adverse remodeling of the heart—The signaling mechanism

Derkachev,

Popov,

Maslov

et al. 2024

Fundamemntal Clinical Pharma

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BackgroundThe high mortality rate of patients with acute myocardial infarction (AMI) remains the most pressing issue of modern cardiology. Over the past 10 years, there has been no significant reduction in mortality among patients with AMI. It is quite obvious that there is an urgent need to develop fundamentally new drugs for the treatment of AMI. Angiotensin 1–7 has some promise in this regard.ObjectiveThe objective of this article is analysis of published data on the cardioprotective properties of angiotensin 1–7.MethodsPubMed, Scopus, Science Direct, and Google Scholar were used to search articles for this study.ResultsAngiotensin 1–7 increases cardiac tolerance to ischemia/reperfusion and mitigates adverse remodeling of the heart. Angiotensin 1–7 can prevent not only ischemic but also reperfusion cardiac injury. The activation of the Mas receptor plays a key role in these effects of angiotensin 1–7. Angiotensin 1–7 alleviates Ca2+ overload of cardiomyocytes and reactive oxygen species production in ischemia/reperfusion (I/R) of the myocardium. It is possible that both effects are involved in angiotensin 1–7‐triggered cardiac tolerance to I/R. Furthermore, angiotensin 1–7 inhibits apoptosis of cardiomyocytes and stimulates autophagy of cells. There is also indirect evidence suggesting that angiotensin 1–7 inhibits ferroptosis in cardiomyocytes. Moreover, angiotensin 1–7 possesses anti‐inflammatory properties, possibly achieved through NF‐kB activity inhibition. Phosphoinositide 3‐kinase, Akt, and NO synthase are involved in the infarct‐reducing effect of angiotensin 1–7. However, the specific end‐effector of the cardioprotective impact of angiotensin 1–7 remains unknown.ConclusionThe molecular nature of the end‐effector of the infarct‐limiting effect of angiotensin 1–7 has not been elucidated. Perhaps, this end‐effector is the sarcolemmal KATP channel or the mitochondrial KATP channel.

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“…12,13 Moreover, research has revealed that knockout of the angiotensinconverting enzyme-2 gene in rats decreases the level of Ang (1)(2)(3)(4)(5)(6)(7), increases the level of Ang II, and aggravates myocardial infarction. 14 In vitro and in vivo experiments have shown that knockout of the Mas gene in mice decreases left ventricular filling pressure, LVdp/dtmax, cardiac output, and the cardiac index. 15 Ang (1-7) reduces the production of reactive oxygen species (ROS) induced by Ang Ⅱ by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin (1-7) Alleviates Postresuscitation Myocardial Dysfunction by Suppressing Oxidative Stress Through the Phosphoinositide 3-Kinase, Protein Kinase B, and Endothelial Nitric Oxide Synthase Signaling Pathway

Zhu

Liu

Huang

et al. 2021

Journal of Cardiovascular Pharmacology

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Continuous angiotensin-(1–7) infusion improves myocardial calcium transient and calcium transient alternans in ischemia-induced cardiac dysfunction rats

Cited by 4 publications

References 27 publications

Renin-Angiotensin-Aldosterone System in Heart Failure: Focus on Nonclassical Angiotensin Pathways as Novel Upstream Targets Regulating Aldosterone

Renin-Angiotensin-Aldosterone System in Heart Failure: Focus on Nonclassical Angiotensin Pathways as Novel Upstream Targets Regulating Aldosterone

Angiotensin 1–7 increases cardiac tolerance to ischemia/reperfusion and mitigates adverse remodeling of the heart—The signaling mechanism

Angiotensin (1-7) Alleviates Postresuscitation Myocardial Dysfunction by Suppressing Oxidative Stress Through the Phosphoinositide 3-Kinase, Protein Kinase B, and Endothelial Nitric Oxide Synthase Signaling Pathway

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