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Iwata, M., Cowling, R.T., Gurantz, D., Moore, C., Zhang, S., Yuan, J.X. and Greenberg, B.H. (2005) Angiotensin-(1-7) Binds, to Specific Receptors on Cardiac Fibroblasts to Initiate Antifibrotic and Antitrophic Effects. American Journal of Physiology, Heart and Circulatory Physiology, 289, H2356-2363.
https://doi.org/10.1152/ajpheart.00317.2005

has been cited by the following article:

• TITLE: A Study of the Correlation between Angiotensin (1-7) and the Histopathological Changes in the Penises of Experimentally Diabetic Rats

  AUTHORS: Abdelaal M. El Kamshoushi, Nagat Sobhy, Suzan F. Helal, Passainte S. Hassaan, Heba Omar

  KEYWORDS: Angiotensin 1-7, Corpus Cavernosum, Erectile Dysfunction, Diabetes Mellitus, Rats

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.8 No.3, March 22, 2018

  ABSTRACT: Background: Diabetes mellitus is an important risk factor for erectile dysfunction. Renin-angiotensin system with its branches Angiotensin II and Angiotensin 1-7 [Ang-(1-7)] are altered in diabetes and could affect erection. So, in this study we determine the level of Ang-(1-7), nitrite (the major nitric oxide metabolite) and histopathological changes in penile tissues of type I diabetic rats. A total of 60 male albino rats were divided into two groups: group I (control) and group II (diabetic) for either 4 weeks in group IIa, or 8 weeks in group IIb. Diabetes was induced by intraperitoneal injection of streptozotocin (60 mg/kg). Penile levels of Ang-(1-7), nitrite and histopathological examination were assessed at 4 and 8 weeks after diabetes induction. Results: Ang-(1-7) and nitrite were decreased in diabetic rats at 4 weeks and continued to be lower at 8 weeks for Ang-(1-7) only. Loss of corpus cavernosum smooth muscle was present in 25% and 85% of rats at 4 and 8 weeks of diabetes respectively (P Conclusion: Diabetes induced progressive decrease in the release of Ang-(1-7) and nitric oxide from the corpora cavernosa in a time-dependent manner with concomitant fibro-muscular changes that end by corporal fibrosis affecting subsequently erectile functions.