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Autocrine/paracrine function of angiotensin 1‐7 in tissue repair during hypertension (856.8)
Author(s) -
Meng Weixin,
Zhao Wenyuan,
Zhao Tieqiang,
Liu Chang,
Chen Yuanjian,
Liu Hongyu,
Sun Yao
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.856.8
Subject(s) - medicine , endocrinology , angiotensin ii , cardiac function curve , cardiac fibrosis , kidney , fibrosis , apoptosis , paracrine signalling , angiotensin converting enzyme 2 , renin–angiotensin system , heart failure , blood pressure , chemistry , receptor , biochemistry , disease , covid-19 , infectious disease (medical specialty)
The purpose of this study is to explore 1) whether circulating AngII affects ACE2/MasR expressions in the hypertensive heart and kidney and 2) whether Ang1‐7 via MasR regulates cardiac repair responses during hypertension. In the first portion of the study, rats received either an AngII infusion (400ng/kg/min) for 4 weeks, leading to hypertension with high circulating AngII; or an aldosterone (ALDO, 0.75μg/h) infusion for 4 weeks, leading to hypertension with low circulating AngII. Cardiac and renal ACE2/MasR expressions were examined. We found that cardiac ACE2 was increased and MasR attenuated in both AngII and ALDO groups. However, renal ACE2 and MasR remained unchanged in both AngII and ALDO‐treated animals. In the second portion, rats received AngII infusion with/without MasR antagonist (A779, 1mg/kg/day) for 4 weeks. The roles of MasR blockade in cardiac inflammation, fibrosis, and apoptosis were examined. Chronic AngII infusion caused scattered cardiac injuries; and A779 co‐treatment exacerbated cardiac injury, resulting in aggravated inflammatory, fibrogenic and apoptotic responses compared to AngII group. Thus, ACE2 and MasR are differently expressed in the hypertensive heart and kidney, which are independent of circulating AngII level. Ang1‐7 involves multiple repair responses and protects the hypertensive heart from remodeling. Grant Funding Source : NIH