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Angiotensin 1‐7 prevents cardiac fibrosis in angiotensin II and DOCA‐salt models of hypertension
Author(s) -
Grobe Justin L,
Mecca Adam P,
Lingis Melissa,
Mao Haoyu,
Katovich Michael J
Publication year - 2006
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.20.4.a305-d
Subject(s) - medicine , angiotensin ii , endocrinology , cardiac fibrosis , ventricle , fibrosis , cardiac hypertrophy , muscle hypertrophy , blood pressure , renin–angiotensin system , left ventricular hypertrophy , saline
Cardiac remodeling is a hallmark of hypertension‐induced pathophysiology. In the current study, the role of angiotensin 1–7 in modulating cardiac remodeling was examined. Hypertension was induced in Sprague‐Dawley rats by either four weeks of angiotensin (Ang) II infusion (100 ng kg −1 min −1 ) or implantation with a deoxycorticosterone acetate pellet (DOCA). DOCA animals were maintained on a 0.9% saline solution. Subgroups were implanted with osmotic minipumps to deliver Ang 1–7 chronically (100 ng kg −1 min −1 ). Indirect blood pressure (BP) was measured weekly, and after four weeks of treatment ventricle size was measured and cross‐sections were stained with Masson’s Trichrome for interstitial collagen deposition. Ang II and DOCA‐salt treatment both caused significant increases in BP, ventricular hypertrophy and fibrosis. Ang 1–7 infusion reversed the collagen deposition effects without any effect on BP or cardiac hypertrophy. These results indicate that Ang 1–7 selectively effects cardiac fibrosis independent of BP and hypertrophy in both Ang II‐dependent and ‐independent models of hypertension.(Predoctoral support for JLG from AHA; Undergrad support for APM from Endo Society)