The cascade, one step at a time
- The kidney releases renin when pressure or salt falls.
- Renin converts angiotensinogen into angiotensin I (inactive).
- ACE (angiotensin-converting enzyme) turns angiotensin I into angiotensin II — the active villain.
- Angiotensin II tightens vessels (raising resistance) and triggers aldosterone, which makes the kidney retain salt and water (raising volume).
So this single RAAS cascade raises BP by both levers at once — tighter vessels and more fluid. Block it and you relax vessels and gently offload fluid together. That dual action, plus protection of the heart and kidney over years, is why RAAS blockers are first-line for so many patients.
Where each drug class cuts the chain
An ACE inhibitor (the '-pril' drugs, e.g. enalapril, ramipril) blocks the ACE enzyme, so less angiotensin II is made. An angiotensin receptor blocker or ARB (the '-sartan' drugs, e.g. losartan) lets angiotensin II form but blocks its receptor, so it cannot act. A mineralocorticoid antagonist (spironolactone) blocks aldosterone at the far end of the chain.
renin -> Ang I --[ACE]--> Ang II --> AT1 receptor --> aldosterone
^ ^ ^
ACE inhibitor ARB aldosterone blocker
(-pril) (-sartan) (spironolactone)The cough, the potassium, and the pregnancy rule
ACE does a second job: it breaks down bradykinin, a peptide that triggers cough. When an ACE inhibitor blocks the enzyme, bradykinin builds up — giving the classic dry, tickly cough in about one in ten people. ARBs do not touch bradykinin, so they rarely cough; switching from a '-pril' to a '-sartan' is the standard fix. This cough is a side effect of mechanism, not an allergy.