Angiotensin-(1-5), an active mediator of renin-angiotensin system, stimulates ANP secretion via Mas receptor

Yu, Longquan; Yuan, Kuichang; Phuong, Hoang Thi Ai; Park, Byung Mun; Kim, Suhn Hee

doi:10.1016/j.peptides.2016.09.009

Cited by 61 publications

(77 citation statements)

References 35 publications

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“…As for the remaining APs, in humans, Ang(2-7) induces mild vasoconstriction, 56 Ang(3-7) is thought to be a centrally acting vasoconstrictor, 57 and Ang1-5 binds MasR and causes vasodilatation and increased natriuretic peptide release. 58 A third important finding of our study is the ability to shift the balance of APs within the RAAS using rhACE2. The counter regulatory role of ACE2 on the maladaptive effects of ACE and AT2(1-8) make ACE2 and its related APs attractive targets for pharmacotherapy.…”

Section: Discussionmentioning

confidence: 80%

Plasma and tissue angiotensin‐converting enzyme 2 activity and plasma equilibrium concentrations of angiotensin peptides in dogs with heart disease

Larouche‐Lebel

Loughran

Oyama

et al. 2019

Veterinary Internal Medicne

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Background Angiotensin‐converting enzyme 2 (ACE2) is a homologue of angiotensin‐converting enzyme (ACE) and produces angiotensin peptides (APs), such as angiotensin 1‐9 and 1‐7 that are vasodilatory and natriuretic, and act to counterbalance angiotensin II. Hypothesis Evidence of ACE2 can be found in tissues and plasma of dogs. Equilibrium concentrations of renin angiotensin aldosterone system (RAAS) APs differ in dogs with heart disease compared to healthy dogs and recombinant human ACE2 (rhACE2) alters relative concentrations of APs. Animals Forty‐nine dogs with and 34 dogs without heart disease. Methods Immunohistochemistry and assays for tissue and plasma ACE2 activity and equilibrium concentrations of plasma RAAS APs were performed. Results Immunolabeling for ACE2 was present in kidney and myocardial tissue. Median plasma ACE2 activity was significantly increased in dogs with congestive heart failure (CHF; 6.9 mU/mg; interquartile range [IQR], 5.1‐12.1) as compared to control (2.2 mU/mg; IQR, 1.8‐3.0; P = .0003). Plasma equilibrium analysis of RAAS APs identified significant increases in the median concentrations of beneficial APs, such as angiotensin 1‐7, in dogs with CHF (486.7 pg/mL; IQR, 214.2‐1168) as compared to those with preclinical disease (41.0 pg/mL; IQR, 27.4‐45.1; P < .0001) or control (11.4 pg/mL; IQR, 7.1‐25.3; P = .01). Incubation of plasma samples from dogs with CHF with rhACE2 increased beneficial APs, such as angiotensin 1‐9 (preincubation, 10.3 pg/mL; IQR, 4.4‐37.2; postincubation, 2431 pg/mL; IQR, 1355‐3037; P = .02), while simultaneously decreasing maladaptive APs, such as angiotensin II (preincubation, 53.4 pg/mL; IQR, 28.6‐226.4; postincubation, 2.4 pg/mL; IQR, 0.50‐5.8; P = .02). Conclusions and Clinical Importance Recognition of the ACE2 system expands the conventional view of the RAAS in the dog and represents an important potential therapeutic target.

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Section: Discussionmentioning

confidence: 80%

Plasma and tissue angiotensin‐converting enzyme 2 activity and plasma equilibrium concentrations of angiotensin peptides in dogs with heart disease

Larouche‐Lebel

Loughran

Oyama

et al. 2019

Veterinary Internal Medicne

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“…Kuba et al [10] demonstrated in mice that SARS-CoV downregulates ACE2 protein (but not ACE) by binding its spike protein, contributing to severe lung injury. This suggests that excessive ACE2 may competitively bind with SARS-CoV-2 not only to neutralize the virus but also rescue cellular ACE2 activity which negatively regulates the renin-angiotensin system (RAS) to protect the lung from injury [12,30]. Indeed, enhanced ACE activity and decreased ACE2 availability contribute to lung injury during acid-and ventilator-induced lung injury [12,31,32].…”

Section: Delivering Excessive Soluble Form Of Ace2mentioning

confidence: 99%

Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target

et al. 2020

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“…Moreover, angiotensin 1-12 has been shown to regulate intracellular calcium transients and left ventri cular contractile function in both normal rats and rats with heart failure (HF) via a chymase dependent and cyclic AMP dependent mechanism 7 . Additionally, angio tensin 1-5 has been found to induce atrial natri uretic peptide (ANP) secretion from isolated perfused rat atria by binding to the Mas receptor and activating the phos phatidylinositol 3kinase-AKT-endothelial NO syn thase pathway 8 . Lastly, angiotensinogen is the precursor for the entire RAS family of peptides, but, to date, no studies have shown that angiotensinogen can elicit direct biological effects on the heart.…”

Section: Components Of the Counter-regulatory Ras Ligandsmentioning

confidence: 99%

“…80. Flores-Munoz, M. et al Angiotensin- (1)(2)(3)(4)(5)(6)(7)(8)(9) attenuates cardiac fibrosis in the stroke-prone spontaneously hypertensive rat via the angiotensin type 2 receptor. Hypertension 59, 300-307 (2012 Inflammatory processes in cardiovascular disease:…”

mentioning

confidence: 99%

Counter-regulatory renin–angiotensin system in cardiovascular disease

et al. 2019

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| The renin-angiotensin system is an important component of the cardiovascular system. Mounting evidence suggests that the metabolic products of angiotensin I and IIinitially thought to be biologically inactive -have key roles in cardiovascular physiology and pathophysiology. This non-canonical axis of the renin-angiotensin system consists of angiotensin 1-7 , angiotensin 1-9, angiotensin-converting enzyme 2, the type 2 angiotensin II receptor (AT 2 R), the proto-oncogene Mas receptor and the Mas-related G protein-coupled receptor member D. Each of these components has been shown to counteract the effects of the classical reninangiotensin system. This counter-regulatory renin-angiotensin system has a central role in the pathogenesis and development of various cardiovascular diseases and, therefore, represents a potential therapeutic target. In this Review , we provide the latest insights into the complexity and interplay of the components of the non-canonical renin-angiotensin system, and discuss the function and therapeutic potential of targeting this system to treat cardiovascular disease.

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Angiotensin-(1-5), an active mediator of renin-angiotensin system, stimulates ANP secretion via Mas receptor

Cited by 61 publications

References 35 publications

Plasma and tissue angiotensin‐converting enzyme 2 activity and plasma equilibrium concentrations of angiotensin peptides in dogs with heart disease

Plasma and tissue angiotensin‐converting enzyme 2 activity and plasma equilibrium concentrations of angiotensin peptides in dogs with heart disease

Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target

Counter-regulatory renin–angiotensin system in cardiovascular disease

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