Peptide directoryHeart, vessels & kidneys

Angiotensin I

The inactive ten, cut from angiotensinogen by renin, one step from the pressor.

Related medicinesAliskiren

Where it comes from

Made in
Formed in blood when renin from the kidney cuts angiotensinogen from the liver
Sent out by
Renin is let out by a fall in blood pressure, salt or volume, and by sympathetic nerves
Acts on
  • Angiotensin-converting enzyme (ACE) in the lung and vessel walls, which makes angiotensin II from it

What it does

  • The substrate for angiotensin II, and nothing else: it has no receptor of its own 1
  • Also cut by ACE2 to angiotensin-(1-9) and by neprilysin to angiotensin-(1-7) 1
  • Made inside tissues as well as in blood, which is what a local renin-angiotensin system means 1

In medicine

  • Plasma renin activity, the test, measures how fast angiotensin I is generated from a patient’s own plasma 1
  • ACE inhibitors (captopril, lisinopril and the rest) stop it from becoming angiotensin II; renin inhibitors stop it from forming at all 2
  • The two classes move the same peptide in opposite directions: angiotensin I rises on an ACE inhibitor and falls on a renin inhibitor 2

Beyond the body’s own use

  • It is not a treatment and is not in trials. Giving it would simply deliver more angiotensin II, since that is all it does 1
  • Its real use is as a measurement: renin activity and the aldosterone-to-renin ratio are both built on how fast it appears, and they are how primary aldosteronism is found
  • What is genuinely open is how much of it is generated inside tissues rather than in the bloodstream, which is the usual explanation for why ACE inhibitors do more than their blood pressure effect predicts 1

Sources

  1. Paul et al., Physiology of local renin-angiotensin systems, Physiological Reviews 2006
  2. Aliskiren (Tekturna), FDA application NDA 021985

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.