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Schiavo, Silvia (2009) Signaling cellulare dell'angiotesina II mediato dai recettori AT2: Relazione con la regolazione del tono vascolare e con il rimodellamento cardiovascolare. Studio nel modello sperimentale della sindrome di Bartter/Gitelman. [Ph.D. thesis]

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Abstract (english)

Biological actions of Ang II are mediated through two distinct different receptors linked to the cell membrane, the AT1R and AT2R (De Gasparo et al, 2000). Most of the effects of Ang II are mediated via the AT1R while AT2R stimulation has been suggested to counteract many actions mediated by AT1R through the induction of vasodilation, antiproliferation and apoptosis but the role of AT2R in these processes remains to be completely elucidated (De Gasparo et al, 2000; Volpe et al, 2003; Stoll et al, 2001; Zhou et al, 2008; Yamamoto et al, 2008; Tsutsumi et al, 1999; Carey et al, 2001; Carey et al, 2000). However, stimulation of this receptor evokes pathways that involve tyrosine or serine/threonine phosphatases. Three such AT2R-associated phosphatases, that interact with the ERK1/2 pathway have been identified: mitogen-activated protein kinase phosphatase 1 (MKP-1) protein phosphatase 2A (PP2A) and SH2 domain-containing phosphatase (SHP-1) (Fischer et al, 1998).The blocking of AT1 receptors by AT1 receptor blockers II greatly increases the plasma concentration of Ang II, which could be available for the stimulation of AT2 receptors and this action could contribute to their antihypertensive activities.
Angiotensin-converting enzyme (ACE) and its homologue ACE2 are responsible for the production of Angiotensin II (Ang II), potent vasopressor and Ang-(1-7), a potent vasodilator, respectively (Ferrario et al, 1997). Because of the opposing actions of Ang 1-7 and Ang II, ACE2 activity may determine blood pressure homeostasis (Ferrario et al, 1997; Iyer et al, 1998; Santos et al, 2007). In fact ACE2 mRNA and protein are markedly reduced in hypertensive rats (Crackower et al, 2002).
ACE2's pathophysiological relevance is supported by its altered expression in cardiac, vascular and renal dysfunctions, by the deleterious effects of ACE2 gene deletion on the cardiovascular and renal systems (Zisman et al, 2003; Ishiyama et al, 2004; Tikellis et al, 2006) as well as the increased plasma, kidney and heart Ang II levels found in ACE2 knockout mice. Together, these data indicate that ACE2 plays a protective role in organs directly related to hypertension and associated diseases (Ferreira et al, 2008).A clinical condition of chronic blockade of AT1 receptor occurs in Bartter's and Gitelman's syndromes, an example of endogenous Ang II AT1R antagonism.Bartter's and Gitelman's syndromes, caused by gene defects in specific kidney transporters and ion channels, present a puzzling clinical picture characterized by hypokalemia, sodium depletion, activation of the renin-angiotensin-aldosterone system (RAAS), with increased plasma levels of Ang II and aldosterone and yet normo/hypotension, reduced peripheral resistance and hyporesponsiveness to pressor agents (Calò et al, 2000). Therefore, we have proffered these patients as a good system to explore the signaling pathways responsible for mediating the signaling of Ang II based on the results of an extensive series of studies that have provided mechanistic explanations for these patients vascular hyporeactivity (Calò et al, 2003; Calò et al, 2001; Calò et al, 2004; Pagnin et al, 2004; Calò et al, 2005; Calò et al, 2005; Pagnin et al, 2005; Davis et al, 2006; Semplicini et al, 2006). Along with these findings has come the recognition that Bartter's and Gitelman's syndromes offer a means to explore the mechanisms responsible for maintenance/controlling vascular tone and cardiovascular remodeling involved in the Ang II signaling mediated by AT2 receptors.

Abstract (italian)

L'Ang II media le sue azioni biologiche attraverso il legame a due distinti recettori legati alla membrana cellulare, i recettori AT1 ed i recettori AT2 (De Gasparo et al, 2000). La maggior parte delle azioni biologiche dell'Angiotensina II, compresa la contrazione della cellula muscolare liscia vascolare, la crescita e l'infiammazione, sono mediate attraverso il legame con i recettori AT1. Evidenze recenti indicano che il recettore AT2 controbilancia questi effetti inducendo vasodilatazione, inibendo la crescita cellulare e l'infiammazione e mediando effetti antiipertrofici ed antiapoptotici (De Gasparo et al, 2000; Volpe et al, 2003; Stoll et al, 2001; Zhou et al, 2008; Yamamoto et al, 2008). L'effetto vasodilatante mediato dai recettori AT2 (Tsutsumi et al, 1999; Carey et al, 2001; Carey et al, 2000) è mediato dal sistema bradichinina/NO/cGMP, mentre la sua azione antirimodellamento è mediata dalla attivazione di fosfatasi che defosforilano la ERK1/2 (Fischer et al, 1998). Il blocco dei recettori AT1 con bloccanti dei recettori AT1 dell'Angiotensina II fa aumentare notevolmente la concentrazione plasmatica di Ang II che si rende così disponibile per lo stimolo dei recettori AT2 e questa azione, peraltro, potrebbe contribuire alla loro attività antiipertensiva. Una condizione clinica sovrapponibile a quella indotta dal blocco cronico del recettore AT1 si verifica nelle Sindromi di Bartter e Gitelman, malattie genetiche caratterizzate da ipokalemia, deplezione di sodio, attivazione del sistema Renina-Angiotensina-Aldosterone (RAAS), con aumentati livelli plasmatici di Ang II e aldosterone, ma normo-ipotensione, ridotte resistenze periferiche ed iporesponsività agli agenti pressori (Calò et al, 2000). Negli studi effettuati su questi pazienti dal nostro gruppo di lavoro, si è dimostrato che il signaling a breve termine dell'Ang II via recettori AT1 è ridotto (Calò et al, 2003; Calò et al, 2001; Calò et al, 2004; Pagnin et al, 2004; Calò et al, 2005; Calò et al, 2005; Pagnin et al, 2005; Davis et al, 2006; Semplicini et al, 2006). La ridotta sensibilità agli effetti dell'Ang II mediati da questi recettori nei pazienti con Sindrome di Bartter e Gitelman, li rende un modello sperimentale umano ideale per la valutazione dei meccanismi cellulari e molecolari mediati dai recettori AT2.
Lo scopo dei nostri studi è stato quello di utilizzare questo modello per poter studiare il segnale mediato dai recettori AT2, prendendo in considerazione inizialmente la via a lungo termine mediata dall'Ang II, analizzando il processo di infiammazione, direttamente collegato allo stress ossidativo e il conseguente processo di rimodellamento cardiovascolare. Una condizione clinica sovrapponibile a quella indotta dal blocco cronico del recettore AT1 si verifica nelle Sindromi di Bartter e Gitelman, malattie genetiche caratterizzate da ipokalemia, deplezione di sodio, attivazione del sistema Renina-Angiotensina-Aldosterone (RAAS), con aumentati livelli plasmatici di Ang II e aldosterone, ma normo-ipotensione, ridotte resistenze periferiche ed iporesponsività agli agenti pressori (Calò et al, 2000). Negli studi effettuati su questi pazienti dal nostro gruppo di lavoro, si è dimostrato che il signaling a breve termine dell'Ang II via recettori AT1 è ridotto (Calò et al, 2003; Calò et al, 2001; Calò et al, 2004; Pagnin et al, 2004; Calò et al, 2005; Calò et al, 2005; Pagnin et al, 2005; Davis et al, 2006; Semplicini et al, 2006). La ridotta sensibilità agli effetti dell'Ang II mediati da questi recettori nei pazienti con Sindrome di Bartter e Gitelman, li rende un modello sperimentale umano ideale per la valutazione dei meccanismi cellulari e molecolari mediati dai recettori AT2.

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EPrint type:Ph.D. thesis
Tutor:D'Angelo, Angela
Supervisor:Calò, Lorenzo
Ph.D. course:Ciclo 21 > Scuole per il 21simo ciclo > SCIENZE MEDICHE, CLINICHE E SPERIMENTALI > SCIENZE NEFROLOGICHE
Data di deposito della tesi:22 January 2009
Anno di Pubblicazione:2009
Key Words:Angiotensina AT2 ACE2 Bartter and Gitelman's Syndrome
Settori scientifico-disciplinari MIUR:Area 05 - Scienze biologiche > BIO/11 Biologia molecolare
Struttura di riferimento:Dipartimenti > pre 2012 - Dipartimento di Scienze Mediche e Chirurgiche
Codice ID:1381
Depositato il:22 Jan 2009
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