Where it comes from
- Made in
- Made from angiotensin II by aminopeptidase A, in blood, kidney and brain
- Sent out by
- Follows angiotensin II
- Acts on
- Adrenal cortex
- Brain (vasopressin release, thirst)
- Kidney
What it does
In medicine
- No medicine and no test of its own. Assays for angiotensin II generally cannot exclude it, since one residue separates them
- It is the reason the brain arm of this system is treated as a separate problem: blocking angiotensin II in the blood does not reach what angiotensin III does inside the brain 1
Beyond the body’s own use
- Firibastat, a brain aminopeptidase A inhibitor designed to stop its formation, failed to lower blood pressure meaningfully in difficult-to-treat and resistant hypertension in the FRESH trial, and its development stopped 2
- That failure is the honest summary of the field: a convincing animal story about brain angiotensin III did not survive a randomised trial in people 12
- Nothing is in trials now and nothing is claimed for the peptide itself
Sources
- Réaux et al., PC18, an aminopeptidase N inhibitor, induces vasopressin release by extending the half-life of brain angiotensin III, Neuroendocrinology 1999
- Zoccali et al., New trials in resistant hypertension: mixed blessing stories, Clinical Kidney Journal 2024
- Paul et al., Physiology of local renin-angiotensin systems, Physiological Reviews 2006
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.