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Angiotensin‐(1–7) prevents cardiac remodeling during angiotensin II‐induced hypertension
Author(s) -
Grobe Justin L,
Mecca Adam P,
Lingis Melissa,
Shenoy Vinayak,
Bolton Tonya A,
Machado Juline M,
Speth Robert C,
Raizada Mohan K,
Katovich Michael J
Publication year - 2007
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.21.6.a896-d
Subject(s) - medicine , angiotensin ii , angiotensin ii receptor type 1 , renin–angiotensin system , endocrinology , cardiac fibrosis , blood pressure , fibrosis , muscle hypertrophy , ventricular remodeling , angiotensin converting enzyme 2 , angiotensin converting enzyme , myocyte , receptor , cardiac myocyte , heart failure , disease , covid-19 , infectious disease (medical specialty)
Cardiac remodeling, including both myocyte hypertrophy and myocardial fibrosis, is an example of end‐organ damage associated with an increased basal activity of the renin‐angiotensin system. We previously demonstrated that lentiviral delivery of angiotensin converting enzyme 2 (ACE2) prevented cardiac remodeling in an angiotensin (Ang) II‐infusion rat model of hypertension. Here, we examined the hypothesis that Ang‐(1–7), the chief enzymatic product of ACE2, can attenuate the pro‐remodeling effects of Ang II. Male Sprague‐Dawley rats were chronically infused with Ang II (100 ng/kg/min), with and without Ang‐(1–7) (100 ng/kg/min) for four weeks. Blood pressure, myocyte diameter, and interstitial fibrosis were significantly increased by Ang II infusion. Ang‐(1–7) co‐infusion caused significant attenuations of myocyte hypertrophy and interstitial fibrosis without affecting the Ang II‐induced hypertension. Cardiac AT 1 and AT 2 receptor populations were unchanged by any treatment. [D‐Ala 7 ]‐Ang‐(1–7) tended to attenuate the anti‐remodeling effects of Ang‐(1–7). Together, these findings indicate that Ang‐(1–7) attenuates Ang II‐induced cardiac remodeling, independent of changes in blood pressure or cardiac angiotensin receptors, and may be partially mediated by the putative Ang‐(1–7) receptor, Mas.