ACE inhibitors vs Angiotensin receptor blockers
How to tell ACE inhibitors and Angiotensin receptor blockers apart when a board question makes them look alike.
ACE inhibitors raise bradykinin; ARBs block the receptor without the same bradykinin cough signal.
Side by side
RAAS blockade with decreased angiotensin II formation plus increased bradykinin, causing cough and angioedema risk.
RAAS blockade at the AT1 receptor without substantial bradykinin buildup, so cough is much less common.
ACE inhibition reduces angiotensin II and decreases bradykinin breakdown.
AT1 receptor blockade prevents angiotensin II signaling while leaving ACE-mediated bradykinin metabolism mostly intact.
Hyperkalemia and creatinine rise can occur; cough or angioedema points toward ACE inhibitor physiology.
Hyperkalemia and creatinine rise can occur; lower cough risk makes ARBs useful when ACE-inhibitor cough appears.
The trap
Both can protect kidneys and both can cause hyperkalemia, hypotension, or creatinine rise.
Watch it explained
Test it nowThe repair move
For RAAS drugs, separate shared aldosterone/renal effects from the ACE-only bradykinin cough and angioedema clue.
Try a free question
CoreA patient with hypertension starts a medication and develops a persistent dry cough with mild hyperkalemia. The drug also reduces angiotensin II and increases bradykinin. Which drug class best fits?
Show answer and explanation
Answer: A. ACE inhibitor. ACE inhibitors decrease angiotensin II formation and increase bradykinin, explaining cough and angioedema risk.
Why the other choices are tempting
- B. ARBs block the angiotensin II receptor and do not increase bradykinin substantially.
- C. Dihydropyridine calcium channel blockers cause vasodilation and edema, not bradykinin cough.
- D. Thiazides can lower potassium and raise calcium rather than causing bradykinin cough.
- E. Beta blockers reduce sympathetic effects and renin release, not ACE-mediated bradykinin breakdown.
Flashcards
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What is the fastest separator for ACE inhibitors vs Angiotensin receptor blockers?
ACE inhibitors raise bradykinin; ARBs block the receptor without the same bradykinin cough signal.
What clue should make you choose ACE inhibitors?
RAAS blockade with decreased angiotensin II formation plus increased bradykinin, causing cough and angioedema risk.
Quick answers
What is the fastest way to tell ACE inhibitors from Angiotensin receptor blockers?
ACE inhibitors raise bradykinin; ARBs block the receptor without the same bradykinin cough signal.
What is the key clue for ACE inhibitors?
RAAS blockade with decreased angiotensin II formation plus increased bradykinin, causing cough and angioedema risk.
What is the key clue for Angiotensin receptor blockers?
RAAS blockade at the AT1 receptor without substantial bradykinin buildup, so cough is much less common.
What is the common trap with ACE inhibitors vs Angiotensin receptor blockers?
Both can protect kidneys and both can cause hyperkalemia, hypotension, or creatinine rise.