Phosphoinositide hydrolysis increase by angiotensin-(1–7) in neonatal rat brain

Pereyra-Alfonso, Susana; Arnaiz, Georgina Rodrı́guez de Lores; Peña, Clara

doi:10.1016/j.regpep.2006.12.005

Cited by 3 publications

(3 citation statements)

References 44 publications

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“…1991), the prostaglandin release in astrocytes (Jaiswal et al. 1991), or the phosphoinositide turnover enhancement in neonatal rat brain (Pereyra‐Alfonso et al. 2007) were blocked by AT 2 antagonists, reflecting an interaction of Ang‐(1–7) with these receptors.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin‐(1–7) through AT₂ receptors mediates tyrosine hydroxylase degradation via the ubiquitin–proteasome pathway

Verrilli

Pirola

Pascual

et al. 2009

Journal of Neurochemistry

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Hypothalamic norepinephrine (NE) release regulates arterial pressure by altering sympathetic nervous system activity. Because angiotensin (Ang) (1–7) decreases hypothalamic NE release and this effect may be correlated with a diminished NE synthesis, we hypothesize that Ang‐(1–7) down‐regulates tyrosine hydroxylase (TH), the rate‐limiting enzyme in catecholamines biosynthesis. We investigated the effect of Ang‐(1–7) on centrally TH activity and expression. TH activity was evaluated by the release of tritiated water from 3H‐l‐tyrosine. TH expression and phosphorylation were determined by western blot. Hypothalami from normotensive or spontaneously hypertensive rats pre‐incubated with Ang‐(1–7) showed a significant decrease in TH specific activity. Ang‐(1–7) caused a decrease in TH phosphorylation at Ser19 and Ser40 residues. The heptapeptide induced a decrease in TH expression that was blocked by an AT2 receptor antagonist and not by an AT1 or Mas receptor antagonist, suggesting the involvement of AT2 receptors. The proteasome inhibitor MG132 blocked the Ang‐(1–7)‐mediated TH reduction. In addition, Ang‐(1–7) increased the amount of TH–ubiquitin complexes, indicating that the Ang‐(1–7)‐mediated TH degradation involves ubiquitin conjugation prior to proteasome degradation. We conclude that Ang‐(1–7) down‐regulates TH activity and expression centrally leading to a decrease in the central NE system activity.

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Section: Discussionmentioning

confidence: 99%

Angiotensin‐(1–7) through AT₂ receptors mediates tyrosine hydroxylase degradation via the ubiquitin–proteasome pathway

Verrilli

Pirola

Pascual

et al. 2009

Journal of Neurochemistry

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“…In these animals, Ang-(1-7) produced a substantial decrease in blood pressure, which was not modified by the Ang-(1-7) receptor antagonist A-779 but was fully blocked by the AT 2 antagonist PD 123319. There are few other reports in which an effect of Ang-(1-7) was blocked or attenuated by PD 123319 but not by A-779 (De Souza et al 2004, Lara et al 2006, Pereyra-Alfonso et al 2007.…”

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

confidence: 96%

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

429

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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“…A great percentage of the AngII receptors in the rostral part of the dorsomedial medulla are AT 2 (angiotensin type 2) subtype, which suggests that Ang-(1-7) binds to AT 2 receptors [59]. the Ang-(1-7)-induced neuronal excitation in the PVN [13], the prostaglandin release in astrocytes [60], the phosphoinositide turnover enhancement in neonatal rat brain [61], NE [noradrenaline (norepinephrine)] release from the hypothalamus of normotensive rats and SHRs [62,63] or TH (L-tyrosine hydroxylase) expression, the rate-limiting enzyme in NE biosynthesis, in neuronal cultures from the hypothalamus of SHRs [64]. the Ang-(1-7)-induced neuronal excitation in the PVN [13], the prostaglandin release in astrocytes [60], the phosphoinositide turnover enhancement in neonatal rat brain [61], NE [noradrenaline (norepinephrine)] release from the hypothalamus of normotensive rats and SHRs [62,63] or TH (L-tyrosine hydroxylase) expression, the rate-limiting enzyme in NE biosynthesis, in neuronal cultures from the hypothalamus of SHRs [64].…”

Section: Receptors Mediating Ang-(1-7) Effectsmentioning

confidence: 99%

Neuromodulatory role of angiotensin-(1–7) in the central nervous system

et al. 2013

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Ang-(1-7) [angiotensin-(1-7)] constitutes an important functional end-product of the RAS (renin-angiotensin system) endogenously formed from AngI (angiotensin I) or AngII (angiotensin II) through the catalytic activity of ACE2 (angiotensin-converting enzyme 2), prolyl carboxypeptidase, neutral endopeptidase or other endopeptidases. Ang-(1-7) lacks the pressor, dipsogenic or stimulatory effect on aldosterone release characteristic of AngII. In contrast, it produces vasodilation, natriuresis and diuresis, and inhibits angiogenesis and cell growth. At the central level, Ang-(1-7) acts at sites involved in the control of cardiovascular function, thus contributing to blood pressure regulation. This action may result from its inhibitory neuromodulatory action on NE [noradrenaline (norepinephrine)] levels at the synaptic cleft, i.e. Ang-(1-7) reduces NE release and synthesis, whereas it causes an increase in NE transporter expression, contributing in this way to central NE neuromodulation. Thus, by selective neurotransmitter release, Ang-(1-7) may contribute to the overall central cardiovascular effects. In the present review, we summarize the central effects of Ang-(1-7) and the mechanism by which the peptide modulates NE levels in the synaptic cleft. We also provide new evidences of its cerebroprotective role.

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Phosphoinositide hydrolysis increase by angiotensin-(1–7) in neonatal rat brain

Cited by 3 publications

References 44 publications

Angiotensin‐(1–7) through AT₂ receptors mediates tyrosine hydroxylase degradation via the ubiquitin–proteasome pathway

Angiotensin‐(1–7) through AT₂ receptors mediates tyrosine hydroxylase degradation via the ubiquitin–proteasome pathway

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

Neuromodulatory role of angiotensin-(1–7) in the central nervous system

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Phosphoinositide hydrolysis increase by angiotensin-(1–7) in neonatal rat brain

Cited by 3 publications

References 44 publications

Angiotensin‐(1–7) through AT2 receptors mediates tyrosine hydroxylase degradation via the ubiquitin–proteasome pathway

Angiotensin‐(1–7) through AT2 receptors mediates tyrosine hydroxylase degradation via the ubiquitin–proteasome pathway

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

Neuromodulatory role of angiotensin-(1–7) in the central nervous system

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Angiotensin‐(1–7) through AT₂ receptors mediates tyrosine hydroxylase degradation via the ubiquitin–proteasome pathway

Angiotensin‐(1–7) through AT₂ receptors mediates tyrosine hydroxylase degradation via the ubiquitin–proteasome pathway