Detailed Explanation
The angiotensins are a family of peptide hormones central to blood pressure regulation. The system works as a cascade: the kidney enzyme renin cleaves the liver protein angiotensinogen to produce angiotensin I (10 amino acids), which is then converted by angiotensin-converting enzyme (ACE) in the lungs to angiotensin II (8 amino acids) — the most powerful vasoconstrictor peptide in the body.
Angiotensin II constricts blood vessels, stimulates aldosterone release from the adrenal glands (causing sodium and water retention), triggers thirst, and stimulates vasopressin release. Together, these actions raise blood pressure and blood volume. Angiotensin III (7 amino acids) has similar but weaker effects.
This pathway is the target of two major drug classes. ACE inhibitors (captopril, lisinopril, enalapril) block the conversion of angiotensin I to II. Angiotensin receptor blockers or ARBs (losartan, valsartan) block the AT1 receptor where angiotensin II acts. Notably, captopril — the first ACE inhibitor — was developed from a peptide found in Brazilian pit viper venom, making it one of the most successful venom-to-drug stories in pharmaceutical history.
Key Facts
- Angiotensin II: most potent endogenous vasoconstrictor
- Renin–angiotensin system controls blood pressure and fluid balance
- ACE inhibitors and ARBs: among the most prescribed drugs worldwide
- Captopril derived from snake venom peptide (Bothrops jararaca)
- Angiotensin I (10 aa) → ACE → Angiotensin II (8 aa)
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