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Interaction of the kallikrein kinin system and vascular endothelial growth factor in left ventricle of mice exposed to intermittent hypoxia (544.1)
Author(s) -
Visniauskas Bruna,
Gomes Guiomar,
Tufik Sergio,
Chagas Jair
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.544.1
Subject(s) - bradykinin , angiogenesis , endocrinology , medicine , intermittent hypoxia , hypoxia (environmental) , ventricle , vascular endothelial growth factor , agonist , receptor , ischemia , chemistry , vegf receptors , obstructive sleep apnea , organic chemistry , oxygen
Intermittent hypoxia (IH) is an experimental model of obstructive sleep apnea syndrome (OSAS). However, the occurrence of cardiac angiogenesis in IH and its related mechanism until now have not yet been clarified. In other models of tissue hypoxia, like ischemia/reperfusion, an interaction between VEGF and the KKS was demonstrated and related to the cardioprotective effects. Aiming to find out evidences for VEGF‐KKS interactions in male mice myocardium after IH, we have performed a RT‐PCR assay in the left ventricle. A significant mRNA level increase in VEGF and B2 bradykinin receptor and a decrease in angiotensin converting enzyme (ACE) were observed after 2 weeks of IH when compared to normoxia group. In models of ischemia/reperfusion it has been suggested that VEGF interaction with B2 receptor agonist is an important step in angiogenesis induction. Our findings allow us to suppose that the increased myocardial expression of VEGF in IH by stimulating the expression of B2 receptor and reducing the expression of ACE could contribute to increase bradykinin, favouring neoangiogenesis in this tissue. Grant Funding Source : Supported by FAPESP (2012/02123‐0)