Angiotensin II (Ang II) is produced in the circulation by the action of angiotensin-converting enzyme (ACE) on angiotensin I, which is itself cleaved from angiotensinogen , a precursor protein synthesised primarily in the liver , by the enzyme renin. The mature octapeptide sequence is Asp-Arg-Val-Tyr-Ile-His-Pro-Phe. Its half-life in plasma is short, typically under two minutes, owing to rapid degradation by angiotensinases and ACE2.
Ang II exerts its physiological effects through two well-characterised receptor subtypes: AT1 and AT2. AT1 receptor activation mediates vasoconstriction, sodium reabsorption in the renal tubule, and stimulation of aldosterone secretion from the adrenal cortex. AT2 receptor signalling is less fully characterised but is associated with vasodilatory and antiproliferative effects in some tissue contexts. Research into these receptor-level distinctions remains active; findings should be interpreted in light of the specific model systems used.
Synthetic analogues of Ang II exist and have been investigated in research and, in some jurisdictions, in closely supervised clinical settings. In Australia, any synthetic peptide analogue of Ang II supplied outside a framework approved by the Therapeutic Goods Administration (TGA) , including supply without inclusion on the Australian Register of Therapeutic Goods (ARTG) or without a valid Special Access Scheme (SAS) or Authorised Prescriber authorisation; is illegal. The TGA actively enforces restrictions on the supply of unapproved peptide products, and supplying them without approval is a criminal offence under the Therapeutic Goods Act 1989 (Cth).
Ang II is classified under the Poisons Standard as a prescription-only substance (Schedule 4) in its approved therapeutic form. Research use is subject to institutional ethics approval and relevant state and territory regulation. This entry describes the endogenous molecule and its physiology only; it does not constitute medical advice and makes no therapeutic claims.
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