Biphasic effects of angiotensin (1-7) and its interactions with angiotensin II in rat aorta

Haulică, I; Bild, Walther; Mihaila, Christian N; Ionita, Teodor; Boisteanu, Corneliu P; Neagu, Bogdan

doi:10.3317/jraas.2003.013

Cited by 20 publications

(14 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, A779, a specific blocker of Ang 1-7, significantly inhibited only the vasodilating response but not the vasoconstricting effects of Ang 1-7. 46 These data confirm that Ang 1-7 is one of the active components of the RAS, involved as a possible counter-regulatory factor for the vasoconstrictor effects of Ang II. They also show that this effect may be limited by the fact that high doses of Ang 1-7 determine vasoconstriction mediated by AT 1 -receptors.…”

supporting

confidence: 74%

Review: Angiotensin Peptides and their Pleiotropic Actions

Haulică

Bild

Şerban

2005

J Renin Angiotensin Aldosterone Syst

Self Cite

View full text Add to dashboard Cite

The concept of tissue renin-angiotensin systems (RAS) is now well established and it is now usual to think in terms of renal and tissue systems. At the same time it has emerged that angiotensin II (Ang II) is not the only biologically active peptide generated by the RAS. At least three others have been identified: the heptapeptide Ang III, the hexapeptide Ang IV and Ang 1-7. Specific receptors exits for the last two peptides. In addition, the range of possible physiological and pathophysiological properties for Ang II has been expanding. The current perception of the RAS is therefore that of a much more complex system than previously believed, with autocrine, paracrine and endocrine properties extending beyond the cardiovascular system. This mini-review focuses on the synthetic pathways of the Ang peptides and describes some of their pleiotropic actions. IntroductionOver the last three decades it has become increasingly clear that bioactive angiotensin peptides can be generated not only in the systemic circulation but also as local hormones in several tissues and organs. Classically, the renin-angiotensin system (RAS) has been considered a hormonal circulating system whose final and bioactive product angiotensin II (Ang II) is produced with participation of two critical enzymes, e.g. renin and the angiotensinconverting enzyme (ACE).

show abstract

supporting

confidence: 74%

Review: Angiotensin Peptides and their Pleiotropic Actions

Haulică

Bild

Şerban

2005

J Renin Angiotensin Aldosterone Syst

Self Cite

View full text Add to dashboard Cite

show abstract

“…16 In addition, Ang-(1-7), which is structurally and functionally very similar to alamandine, also has biphasic effects on rat aortic rings. 17 In our study, the HR of the rats was not significantly influenced by alamandine. In addition, the early pressor Compared to the normotensive rats, the 2K1C hypertensive rats had higher basal LVEDP values.…”

Section: Resultsmentioning

confidence: 63%

Differences in Cardiovascular Responses to Alamandine in Two-Kidney, One Clip Hypertensive and Normotensive Rats

Javanmardi

Kouhpayeh

et al. 2017

Circ J

View full text Add to dashboard Cite

angiotensin II type 1 receptor (AT1R) blockers. These drugs block angiotensin II (Ang II) -the primary active peptide in the RAS, which has many effects on blood vessels, the heart, the brain and the kidneys -from activating AT1R. AT1R is one of the two well-characterized receptors that Ang II activates (in addition to angiotensin II type 2 receptor (AT2R)). 3 Losartan is an angiotensin receptor blocker, 4 which mainly antagonizes AT1R, while PD123319 can block AT2R and Mas-related G protein-coupled receptor D (MrgD) receptors. 5 Recently, numerous researchers have shown that the RAS has additional complex multifunctional peptides, enzymes and receptors. The discovery of the ACE2/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, 6,7 which counterbalances several functions of the ACE/Ang II/AT1R axis, has highlighted the complexity of the RAS. The ACE2/Ang-(1-7)/ Mas receptor axis acts as a counter-regulatory axis. 7 It involves the heptapeptide peptide known as Ang-(1-7), which acts through a G-protein-coupled receptor called Mas. 7 Ang-(1-7) can be hydrolyzed from Ang II by the action of peptidases such as ACE2 and prolyl endopepti-D espite major progress in the research on the pathogenesis and management of hypertension and other aspects of cardiometabolic disease, these conditions underlie a significant number cases of morbidity and mortality due to cardiovascular and chronic kidney disease. It is predicted that there will be an increase in the hypertension prevalence rate in the United States (US). Currently, this condition affects 29% of the population in this country; that is, ~65 million individuals. 1 The significance of the renin-angiotensin system (RAS) in the development of hypertension and cardiovascular disease is well known. 2 Chronic RAS activation is a significant causal factor associated with the gradual malfunction of organs such as blood vessels, the kidneys and the heart. 2 These consequences of RAS activation have encouraged the development of medicines that can deactivate the RAS and thereby prevent the associated pathologies. The first class of drugs aimed at RAS inhibition are known as angiotensin-converting enzyme (ACE1) inhibitors, and they came on the market in the late 1970 s. Background: Alamandine is a newly discovered component of the renin-angiotensin system, which regulates blood pressure. In this study, the effect of alamandine on cardiovascular parameters in two-kidney, one clip (2K1C) hypertensive rats and normotensive rats, and the possible roles of the angiotensin II type 1 receptor (AT1R) and the PD123319-sensitive receptors in mediating this effect was investigated.

show abstract

“…In addition, hypertensive effects of angiotensin(1-7) through AT 1 R stimulation have been described [27]. Differences in experimental models and protocols, such as in vitro versus in vivo studies, the use of anaesthetics, different dietary sodium intakes [28,29], water loading [26], and different angiotensin(1-7)-doses [30], may be responsible for these discrepancies. Because the effects of angiotensin(1-7) on renal vascular physiology are poorly characterized, we aim to establish the role of angiotensin(1-7) at several levels of the renal vasculature.…”

Section: Introductionmentioning

confidence: 98%