It is well-established that Ang-(1-7) counteracts the effects of Ang II in the periphery, while stimulating vasopressin release and mimicking the activity of Ang II in the brain, through interactions with various receptors. The rapid metabolic inactivation of Ang-(1-7) has proven to be a limitation to therapeutic administration of the peptide. To circumvent this problem, Alves et al. (Clinical Science (2021) 135(18), https://doi.org/10.1042/CS20210599) developed a new transgenic rat model that overexpresses an Ang-(1-7)-producing fusion protein. In this commentary, we discuss potential concerns with this model while also highlighting advances that can ensue from this significant technical feat.

Keywords:
Angiotensin-(1-7), Cardiovascular System, Renin-Angiotensin System, Sympathetic Nervous System, Transgenic Rat, Vasopressin
Subjects:
Biochemical Techniques & Resources, Cardiovascular System & Vascular Biology, Gene Expression & Regulation, Pharmacology & Toxicology, Protein Engineering
© 2021 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2021
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