Angiotensin-(1–7) Modulates Angiotensin II-Induced Vasoconstriction in Human Mammary Artery

Mendonça, Luís; Mendes-Ferreira, Pedro; Bento-Leite, Ana; Cerqueira, Rui J; Amorim, Mário Jorge; Pinho, Paulo; Brás-Silva, Carmen; Leite‐Moreira, Adelino F.; Castro-Chaves, Paulo

doi:10.1007/s10557-014-6555-4

Cited by 20 publications

(19 citation statements)

References 46 publications

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“…The same authors (560) demonstrated that the effect of ANG-(1-7) infusion on renal blood flow was also reduced in stenotic kidneys. Mendonça et al (359) have recently demonstrated that ANG-(1-7) significantly attenuates ANG IIinduced vasoconstriction in human mammary arteries from patients submitted to coronary revascularization, probably through direct effects on smooth muscle cells, since this action was not abolished by A-779, PD123177, or endothelium removal.…”

Section: As For Antithrombotic Effects Experiments Performed Inmentioning

confidence: 99%

The ACE2/Angiotensin-(1–7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1–7)

Santos

Sampaio

Alzamora

et al. 2018

Physiological Reviews

887

906

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The renin-angiotensin system (RAS) is a key player in the control of the cardiovascular system and hydroelectrolyte balance, with an influence on organs and functions throughout the body. The classical view of this system saw it as a sequence of many enzymatic steps that culminate in the production of a single biologically active metabolite, the octapeptide angiotensin (ANG) II, by the angiotensin converting enzyme (ACE). The past two decades have revealed new functions for some of the intermediate products, beyond their roles as substrates along the classical route. They may be processed in alternative ways by enzymes such as the ACE homolog ACE2. One effect is to establish a second axis through ACE2/ANG-(1-7)/MAS, whose end point is the metabolite ANG-(1-7). ACE2 and other enzymes can form ANG-(1-7) directly or indirectly from either the decapeptide ANG I or from ANG II. In many cases, this second axis appears to counteract or modulate the effects of the classical axis. ANG-(1-7) itself acts on the receptor MAS to influence a range of mechanisms in the heart, kidney, brain, and other tissues. This review highlights the current knowledge about the roles of ANG-(1-7) in physiology and disease, with particular emphasis on the brain.

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Section: As For Antithrombotic Effects Experiments Performed Inmentioning

confidence: 99%

The ACE2/Angiotensin-(1–7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1–7)

Santos

Sampaio

Alzamora

et al. 2018

Physiological Reviews

887

906

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“…Secondly, SW increased the blood pressure in the WKY rats and exacerbated the blood pressure in the SHR. This is mainly attributed to the increase in the levels of ANG-II in the serum caused by metabolic disorders, as well as increased expression of AGTR and decreased expression of eNOS in the carotid artery, ultimately resulting in increased blood pressure [60][61][62] . In addition, metabolic disorders trigger an elevation in the levels of IL-6, resulting in an increase in the inflammatory response of the blood vessel [63,64] .…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, the decrease in compliance was primarily associated with the increase in the content of collagen fiber in the vessel wall [67][68][69] , and the imbalance in the ratio of eNOS to AGTR expression in the vessel wall. [60][61][62] However, with respect to the blood flow velocity, the effects of SW on the carotid arteries of the two types of rats were not identical. In the WKY rats, SW reduced the diameter of the carotid artery and increased the blood flow velocity.…”

Section: Discussionmentioning

confidence: 99%

Effects of Shift Work on the Carotid Artery and Cerebral Blood Flow of Spontaneously Hypertensive Rats and Wistar-Kyoto Rats

Wang

Zhang

et al. 2019

Preprint

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Objective: The objective was to investigate the effects of shift-work (SW) on the carotid arteries. Methods: This study used two inverted photoperiods (inverted light:dark [ILD]16:8 and ILD12:12) to create the SW model. We recorded the rhythm and performed serological tests, carotid ultrasound, magnetic resonance imaging, and carotid biopsy. Results: SW induced elevated blood pressure and increased angiotensin-II, apolipoprotein E, blood glucose, and triglycerides. SW increased the carotid intima-media thickness. SW led to the development of carotid arterial thrombosis, reduced cerebral blood flow, and increased the number of collagen fibers, expression of angiotensin receptor and low-density lipoprotein receptor in the carotid arteries. SW decreased 3-hydroxy-3-methylglutaryl-CoA reductase and nitric oxide. SW induced the atherosclerotic plaque in the aorta. Multiple results of SHR were worse than WKY rats. Conclusion: SW can induce metabolic disorders and elevated blood pressure. SW can cause intima-media thickening of the carotid artery and aorta atherosclerosis. SW may result in carotid arterial thrombosis and affect cerebral blood flow.Hypertension can aggravate the adverse effects of SW.

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“…Unexpectedly, pre‐incubation with the specific MAS1 antagonist A‐779 did not abolish this effect of AngII. Furthermore, the Ang(1–7) effect observed in HMA was not altered by the AT 2 receptor antagonist PD123177, indicating a pharmacologically distinct receptor in HMA (Mendonca et al, ).…”

Section: Confusing Evidencementioning

confidence: 99%

“…There is evidence in the literature for additional receptors mediating the effects of Ang(1–7) (Figure ). For example, the AT 2 receptor was shown to bind Ang(1–7) (De Souza et al, ; Walters et al, ) and Ang(1–7) signals through AT 2 receptors in some studies (Jones et al, ; Sipahi et al, ; Ohshima et al, ), although this is not replicated in all settings (Lautner et al, ; Mendonca et al, ; Tetzner et al, ). De‐orphanization efforts on the MAS1‐related GPCR (MRGPR) family have uncovered potential new receptors for consideration in the ACE2/Ang(1–7) pathway (Gembardt et al, ; Solinski et al, ).…”

Section: Introductionmentioning

confidence: 99%

Significance of angiotensin 1–7 coupling with MAS1 receptor and other GPCRs to the renin‐angiotensin system: IUPHAR Review 22

Karnik

Singh

Tirupula

et al. 2017

British J Pharmacology

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This paper, written by members of the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR) subcommittees for the angiotensin receptors, confirms the existing nomenclature for these receptors and reviews our current understanding of their structure, pharmacology and functions, and their likely physiological roles in health and disease. More information on these receptor families can be found in the Concise Guide to PHARMACOLOGY Angiotensins are a group of hormonal peptides and include angiotensin II and angiotensin 1-7 produced by the renin angiotensin system. The biology, pharmacology and biochemistry of the receptors for angiotensins were extensively reviewed recently. In the review, the receptor nomenclature committee was not emphatic on designating MAS1 as the angiotensin 1-7 receptor on the basis of lack of classical G protein signalling and desensitization in response to angiotensin 1-7, as well as a lack of consensus on confirmatory ligand pharmacological analyses. A review of recent publications (2013-2016) on the rapidly progressing research on angiotensin 1-7 revealed that MAS1 and two additional receptors can function as 'angiotensin 1-7 receptors', and this deserves further consideration. In this review we have summarized the information on angiotensin 1-7 receptors and their crosstalk with classical angiotensin II receptors in the context of the functions of the renin angiotensin system. It was concluded that the receptors for angiotensin II and angiotensin 1-7 make up a sophisticated cross-regulated signalling network that modulates the endogenous protective and pathogenic facets of the renin angiotensin system.

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Angiotensin-(1–7) Modulates Angiotensin II-Induced Vasoconstriction in Human Mammary Artery

Cited by 20 publications

References 46 publications

The ACE2/Angiotensin-(1–7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1–7)

The ACE2/Angiotensin-(1–7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1–7)

Effects of Shift Work on the Carotid Artery and Cerebral Blood Flow of Spontaneously Hypertensive Rats and Wistar-Kyoto Rats

Significance of angiotensin 1–7 coupling with MAS1 receptor and other GPCRs to the renin‐angiotensin system: IUPHAR Review 22

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