Dias, J;
Axelband, F;
Lara, LS;
Muzi-Filho, H;
Vieyra, A;
(2017)
Is angiotensin-(3–4) (Val-Tyr), the shortest angiotensin II-derived peptide, opening new vistas on the renin–angiotensin system?
Journal of the Renin-Angiotensin-Aldosterone System
, 18
(1)
10.1177/1470320316689338.
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Abstract
Angiotensin-(3−4) (Ang-(3−4) or Val-Tyr) is the shorter angiotensin (Ang) II-derived peptide, formed through successive hydrolysis that culminates with the release of Val-Tyr as a dipeptide. It is formed both in plasma and in kidney from Ang II and Ang III, and can be considered a component of the systemic and organ-based renin–angiotensin system. It is potently antihypertensive in humans and rats, and its concerted actions on proximal tubule cells culminate in the inhibition of fluid reabsorption, hyperosmotic urinary excretion of Na+. At the renal cell signaling level, Ang-(3−4) counteracts Ang II-type 1 receptor-mediated responses by acting as an allosteric enhancer in Ang II-type 2 receptor populations that target adenosine triphosphate-dependent Ca2+ and Na+ transporters through a cyclic adenosine monophosphate-activated protein kinase pathway.
| Type: | Article |
|---|---|
| Title: | Is angiotensin-(3–4) (Val-Tyr), the shortest angiotensin II-derived peptide, opening new vistas on the renin–angiotensin system? |
| Open access status: | An open access version is available from UCL Discovery |
| DOI: | 10.1177/1470320316689338 |
| Publisher version: | https://doi.org/10.1177%2F1470320316689338 |
| Additional information: | This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page(https://us.sagepub.com/en-us/nam/open-access-at-sage). |
| Keywords: | Ang-(3–4), local renal RAS, AT1R/AT2R heterodimer dissociation, cyclic adenosine monophosphate-dependent protein kinase, Na+-ATPase, hyperosmotic urinary Na+ excretion, antihypertensive action |
| UCL classification: | UCL UCL > Provost and Vice Provost Offices UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute > Research Department of Haematology |
| URI: | https://discovery.ucl.ac.uk/id/eprint/10064912 |
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