Angiotensin II and angiotensin-(1–7) inhibit the inner cortex Na+-ATPase activity through AT2 receptor

Souza, A.M. De; Lopes, Anibal Gil; Pizzino, C.P; Fossari, R.N; Miguel, Natalina; Cardozo, F.P; Abi-Abib, Raquel de Carvalho; Fernandes, Mário Marques; Santos, D.P.A.; Caruso-Neves, Celso

doi:10.1016/j.regpep.2004.03.005

Cited by 67 publications

(50 citation statements)

References 39 publications

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“…22 Oudot et al have demonstrated AT 1 -dependent vasoconstriction and nicotinamide adenine dinucleotide phosphate oxidase activation by the heptapeptide. 32 In addition to these AT 1 -mediated effects, other publications have demonstrated AT 2 -mediated effects of Ang-(1-7), for example, on the Na + -ATPase of the inner 33 and outer cortex. 34 Furthermore, Walters et al 35 have demonstrated that vasorelaxant effects of Ang-(1-7) can be mediated by AT 2 .…”

Section: Impact Ofmentioning

confidence: 97%

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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Section: Impact Ofmentioning

confidence: 97%

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

et al. 2012

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“…In this context, Ang-(1-7) seems to limit transcellular sodium flux by modulating the activity of transporters via phospholipase A2 activation in tubular epithelial cells (Andreatta-van Leyen et al 1993). Moreover, this heptapeptide appears to be a potent inhibitor of Na C -K C -ATPase activity in the renal cortex and in isolated convoluted proximal tubules (Handa et al 1996, Lopez Ordieres et al 1998, Burgelova et al 2002, De Souza et al 2004, Dilauro & Burns 2009, Pinheiro & Simoes 2012. This inhibitory effect is reversed by the AT 2 receptor antagonist PD 123319 in a dose-dependent manner in the inner cortex basolateral membrane from pig kidney.…”

Section: Vascular Actions Of the Ace2/ang-(1-7)/mas Axismentioning

confidence: 99%

Angiotensin-converting enzyme 2, angiotensin-(1–7) and Mas: new players of the renin–angiotensin system

Santos

Ferreira

Verano‐Braga

et al. 2012

Journal of Endocrinology

439

369

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Angiotensin (Ang)-(1-7) is now recognized as a biologically active component of the reninangiotensin system (RAS). Ang-(1-7) appears to play a central role in the RAS because it exerts a vast array of actions, many of them opposite to those attributed to the main effector peptide of the RAS, Ang II. The discovery of the Ang-converting enzyme (ACE) homolog ACE2 brought to light an important metabolic pathway responsible for Ang-(1-7) synthesis. This enzyme can form Ang-(1-7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1-9) with subsequent Ang-(1-7) formation by ACE. In addition, it is now well established that the G protein-coupled receptor Mas is a functional binding site for Ang-(1-7). Thus, the axis formed by ACE2/Ang-(1-7)/Mas appears to represent an endogenous counterregulatory pathway within the RAS, the actions of which are in opposition to the vasoconstrictor/ proliferative arm of the RAS consisting of ACE, Ang II, and AT 1 receptor. In this brief review, we will discuss recent findings related to the biological role of the ACE2/Ang-(1-7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism. In addition, we will highlight the potential interactions of Ang-(1-7) and Mas with AT 1 and AT 2 receptors.

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“…When Ang 1-7 and A779 were used at equimolar doses, Ang 1-7 antagonist failed to block Ang 1-7-induced depressor response against AT1R blockade; suggesting that Ang 1-7 may act via the AT2R (43). Therefore, there is a complex interaction between RAS receptors (4, 6), and some actions of Ang 1-7 may also be blocked by AT1R (1,5) or AT2R antagonists (9); suggesting a crosstalk between the MasR and Ang II receptors (20). Other data indicated that the antidiuretic effect of AVE0991 that mimics the effects of Ang 1-7 was completely blocked by PD123319 and partially blocked by losartan (43).…”

Section: Discussionmentioning

confidence: 99%

Role of Mas receptor antagonist (A779) in renal hemodynamics in condition of blocked angiotensin II receptors in rats

Mansoori

Oryan

Nematbakhsh

2016

Acta Physiologica Hungarica

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The vasodilatory effect of angiotensin 1–7 (Ang 1-7) is exerted in the vascular bed via Mas receptor (MasR) gender dependently. However, the crosstalk between MasR and angiotensin II (Ang II) types 1 and 2 receptors (AT1R and AT2R) may change some actions of Ang 1-7 in renal circulation. In this study by blocking AT1R and AT2R, the role of MasR in kidney hemodynamics was described. In anaesthetized male and female Wistar rats, the effects of saline as vehicle and MasR blockade (A779) were tested on mean arterial pressure (MAP), renal perfusion pressure (RPP), renal blood flow (RBF), and renal vascular resistance (RVR) when both AT1R and AT2R were blocked by losartan and PD123319, respectively. In male rats, when AT1R and AT2R were blocked, there was a tendency for the increase in RBF/wet kidney tissue weight (RBF/KW) to be elevated by A779 as compared with the vehicle (P=0.08), and this was not the case in female rats. The impact of MasR on renal hemodynamics appears not to be sexual dimorphism either when Ang II receptors were blocked. It seems that co-blockade of all AT1R, AT2R, and MasR may alter RBF/ KW in male more than in female rats. These findings support a crosstalk between MasR and Ang II receptors in renal circulation.

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Angiotensin II and angiotensin-(1–7) inhibit the inner cortex Na+-ATPase activity through AT2 receptor

Cited by 67 publications

References 39 publications

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

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

Angiotensin-converting enzyme 2, angiotensin-(1–7) and Mas: new players of the renin–angiotensin system

Role of Mas receptor antagonist (A779) in renal hemodynamics in condition of blocked angiotensin II receptors in rats

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