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- Title
Angiotensin-(1-7) prevents cardiac remodeling during angiotensin II- induced hypertension.
- Authors
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.
- Abstract
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 AT1 and AT2 receptor populations were unchanged by any treatment. [D-Ala7]-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.
- Subjects
ANGIOTENSINS; VENTRICULAR remodeling; ANGIOTENSIN II; RENIN-angiotensin system; ANGIOTENSIN converting enzyme; HYPERTENSION; HYPERTROPHY; LABORATORY rats
- Publication
FASEB Journal, 2007, Vol 21, Issue 6, pA896
- ISSN
0892-6638
- Publication type
Article
- DOI
10.1096/fasebj.21.6.a896-d