Abstract 356: Angiotensin II as a Paracrine Factor in Heart Environment
Besides its potent vasoconstrictor action, the Angiotensin II (Ang II) has other important biological roles as autocrine and paracrine actions, being fundamental in cardiovascular homeostasis. Changes in the levels of this substance in the pericardial fluid (PF) are associated with the development of cardiovascular diseases. The aim of this study was to evaluate the presence of members of the classical and alternative pathways of the Renin Angiotensin System (RAS), as well as one of its main effectors peptides, Ang II, in PF of patients with coronary artery disease and assess the role of Ang II as a factor able to promote the process of epithelial-mesenchymal transition epicardial mesothelial cells in genetically modified mice. Male and female patients with coronary artery disease and controls patients were involved in this study. The ELISA’s results showed significant amounts of Ang II, Angiotensin Converting Enzyme (ACE) and chymase in PF coronary artery disease male patients. Chymase positive mast cells were identified by immunohistochemical and quantitative analysis demonstrated a greater density of mast cells in this group. Expression of AT1 and AT2 was detected by immunohistochemistry in patients of male and female groups with coronary artery disease and controls. The scaling of the parietal mesothelium is a process seen in all groups, although when quantified showed no significant differences between them. Ang II was not able to increase the epithelial-mesenchymal transition of the epicardial cells in infarcted mice genetically modified. The presence of constituents of the classical and alternative pathways of RAS in the PF suggest an important role for this fluid as a modulator of cardiac functions. Specifically in relation to Ang II, their biological roles in the cardiovascular system still need to be further investigated. The identification in the cardiovascular microenvironment of paracrine factors and your action mechanisms, which stimulate and promote cardiac repair, may allow a better understanding of heart disease and the development of new therapies.
Author Disclosures: I.C.C. Pereira: None. M.P. Rodrigues: None. L.G.L. Teodoro: None. F.F. Vieira: None. R.A.S. Gomes: None.
- © 2015 by American Heart Association, Inc.