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Master's Dissertation
DOI
10.11606/D.42.2007.tde-28012008-103638
Document
Author
Full name
Rodrigo Azevedo Loiola
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2007
Supervisor
Committee
Carvalho, Maria Helena Catelli de (President)
Franco, Maria do Carmo Pinho
Rossoni, Luciana Venturini
Title in Portuguese
Venoconstrição induzida por angiotensina  II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2.
Keywords in Portuguese
Angiotensina II
Hipertensão
Sistema renina angiotensina
Sistema venoso.
Abstract in Portuguese
Neste estudo, avaliamos e caracterizamos o efeito de Ang II em leito venular mesentérico (LVM) e anéis de veia porta (AVP) de wistar e SHR. A reatividade vascular para Ang II foi estudada na presença e ausência de diferentes antagonistas para elucidar os mecanismos envolvidos na venoconstrição induzida por Ang II. Nossos resultados sugerem que a Ang II induz venoconstrição através da ativação de receptores AT1 e AT2 em Wistar e receptor AT1 em SHR. Essa venoconstrição parece ser contrabalanceada pelo receptor B2 em ambas as espécies. NO contribue para este efeito em wistar e metabólitos da COX em SHR. Há redução da venoconstrição induzida por Ang II em AVP de SHR que pode estar relacionado a redução da expressão protéica de receptores AT2. Esses resultados indicam diferentes mecanismos de regulação do tônus venoso de ratos wistar e SHR em resposta a Ang II que podem ter relevância no controle do retorno venoso e débito cardíaco.
Title in English
Angiotensin II induced venoconstriction in normotensive and hypertensive rats: study of action mechanisms, localization and expression of AT1 and AT2 receptors.
Keywords in English
Angiotensin II
Hypertension
Renin angiotensin system
Venous system.
Abstract in English
In this study we have evaluated and characterized the effect of Ang II in the isolated perfused mesenteric venular bed (MVB) and portal vein rings (PVR) of SHR and wistar rats. Vascular reactivity to Ang II was studied in the absence and presence of different antagonists to elucidate the mechanisms involved in Ang II-induced venoconstriction. Our results suggest that Ang II induces venoconstriction by activation of AT1 and AT2 receptors in wistar and AT1 receptor in SHR. These venoconstriction seems to be counterbalanced by B2 receptor in both species. NO might contribute to this effect in wistar and COX metabolites in SHR. There is a decrease in Ang II induced venoconstriction in PVR of SHR that might be related to the decrease of protein expression of AT2 receptor. These results indicate different mechanisms of regulation of venous tonus of the SHR and wistar rats induced by Ang II that can be relevant in the control of the venous return and cardiac output.
 
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Publishing Date
2008-02-08
 
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