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Stimulation of ANP secretion by Angiotensin‐(1–9) via Angiotensin Type 2 Receptor
Author(s) -
Cha Seung Ah,
Park Byung Mun,
Oh YoungBin,
Gao Shan,
Kim Suhn Hee
Publication year - 2013
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.27.1_supplement.lb688
Subject(s) - medicine , endocrinology , angiotensin ii , atrial natriuretic peptide , chemistry , receptor , secretion , renin–angiotensin system , biology , blood pressure
Renin‐angiotensin system (RAS) plays an essential role in cardiovascular homeostasis. The peptide hormone angiotensin II (Ang II), generated by angiotensin converting enzyme (ACE), mainly regulates cardiovascular system via its receptors. More recently, we have reported that Ang‐(1–7) stimulates ANP secretion via Mas receptor. However, Ang‐(1–9), converted from Ang I by ACE 2, is still unknown. The aim of the present study is to determine whether Ang‐(1–9) stimulates ANP secretion using isolated perfused beating atria and to find out its signaling pathway. Ang‐(1–9) augmented ANP secretion and concentration in a dose‐dependent manner. Ang‐(1–9)‐induced ANP secretion (about 60% increase by 3 uM) was attenuated by the pretreatment with Ang II type 2 receptor (AT2R) antagonist but not by AT1R or Mas receptor antagonist. In addition, pretreatment with inhibitors of phosphatidylinositol 3 kinase(PI3K), protein kinase B (Akt), endothelial nitric oxide synthase (eNOS) or guanylyl cyclase (GC), blocked the attenuation of ANP secretion by Ang‐(1–9). However, Ang‐(1–9) did not influence atrial contractility and ECF translocation. These results suggest that Ang‐(1–9) stimulates ANP secretion via AT2R, PI3K, Akt, eNOs, GC pathway. We try to do further study to find out the signaling mechanism involved these responses. Supported by the National Research Foundation (2012–0009322 )