ARBs
High-yield Verified · Oct 2026Prototype: losartan
ARBs are a class of medications used for hypertension.
Medical view → mechanisms, drug comparisons and Step 1 pharmacology
Angiotensin II receptor blockers. Same RAAS target as ACE inhibitors, one step further downstream.
How it works in the body
The system involved, what goes wrong, and how the drug and body interact.
01 The RAAS, one step further down
The renin-angiotensin-aldosterone system (RAAS) raises blood pressure and volume, ending in the powerful hormone angiotensin II, which constricts vessels and drives aldosterone-mediated sodium and water retention (see ACE Inhibitors for the full cascade).
ACE inhibitors work by making less angiotensin II. ARBs take a different route: they let angiotensin II be made but block the receptor (the AT₁ receptor) it acts on. The downstream result is the same — vessels relax, aldosterone falls, blood pressure drops — but the mechanism sidesteps the ACE inhibitor’s signature problem.
02 Why "no cough" matters — the bradykinin difference
ACE does two jobs: it makes angiotensin II and it breaks down bradykinin. Blocking ACE lets bradykinin pile up, causing the nagging dry cough (roughly 5–20% of patients) and, rarely, angioedema. Because ARBs act at the receptor and leave ACE — and therefore bradykinin — untouched, they are not likely to cause the cough. That makes them the standard substitute for a patient who cannot tolerate an ACE inhibitor.
The trade-offs are otherwise similar: because they still suppress aldosterone, ARBs raise potassium and drop glomerular filtration pressure, and — critically — they carry the same fetal-toxicity boxed warning.
Drug names
Indications
- Hypertension
- Heart failure & post-MI (ACE-inhibitor alternative)
- Diabetic nephropathy / chronic kidney disease (renal protection)
Mechanism of action
Selectively block the angiotensin II type-1 (AT₁) receptor, preventing angiotensin II from causing vasoconstriction and aldosterone release — lowering blood pressure and reducing sodium/water retention. Bradykinin metabolism is unaffected (hence cough is rare — about the placebo rate).
Therapeutic effects — what you'll see working
The effects — and how you judge them — mirror ACE inhibitors: a gradual blood-pressure fall, mostly within 1–2 weeks and maximal by about 3–6 weeks, plus protective benefit in heart failure and diabetic kidney disease. They treat hypertension and are the suggested alternative for the ACE-intolerant patient.
- ↓ Blood pressure
- Blocking AT₁ removes angiotensin II–driven vasoconstriction and lowers aldosterone (less fluid retention) — so both resistance and volume fall, gradually over days to weeks.
- Renal protection
- Reducing angiotensin II effect at the glomerulus lowers intraglomerular pressure, slowing progression of diabetic and chronic kidney disease (so a creatinine rise of up to 30% is generally expected).
- Rarely causes dry cough
- Because bradykinin is not affected, ARBs avoid the ACE-inhibitor cough — a common reason a patient is switched to this class.
Adverse effects
The side effects come from too little angiotensin II effect — the same aldosterone-loss story as ACE inhibitors (hyperkalemia, hypotension, rising creatinine) — with far fewer bradykinin-type problems (cough, angioedema).
Interactions
Contraindications
The contraindications match ACE inhibitors — situations where removing angiotensin II effect is dangerous — because the end target is the same.
When to hold
Assess before giving — these findings mean hold the dose and act.
Nursing considerations
The RN-specific layer — each action paired with the reason it matters.
Common questions
What are ARBs used for?
How do ARBs work?
What are the serious side effects of ARBs?
When should a nurse hold ARBs, and what safety checks apply?
Conditions treated
The DCM alternative to an ACE inhibitor; same cautions — avoided or used very cautiously in HCM, contraindicated in pregnancy.
The RAS-inhibition pillar for patients who can’t tolerate an ACE inhibitor (classically because of cough).
First-line with the same compelling-indication logic as ACE inhibitors (heart failure, proteinuric CKD, diabetes with albuminuria) — and the same rule: ACE inhibitor or ARB, never both.
First-line alternative to an ACE inhibitor under the same KDIGO recommendation — one RAS inhibitor, never an ACEi–ARB combination.
Hyperkalemia caution with tacrolimus (StatPearls).
See also
Slow heart rate & lower BP by blocking β-adrenergic receptors. Watch for bradycardia.
Lower BP by blocking angiotensin conversion. Classic dry cough & angioedema risk.
Lower LDL cholesterol via HMG-CoA reductase inhibition. Monitor for myopathy.
Injectable antibodies that protect the liver’s LDL receptors, cutting LDL cholesterol by about half and lowering cardiovascular events. Given subcutaneously every 2–4 weeks.
PPAR-α agonists that mainly lower triglycerides — used with diet for severe hypertriglyceridemia — with muscle, gallbladder, liver and kidney risks, highest for gemfibrozil combined with a statin.
Non-absorbed resins that trap bile acids in the gut, forcing the liver to use cholesterol and pull LDL from the blood. Constipation, drug binding and rising triglycerides are the issues to manage.
Sources
- COZAAR (losartan) — boxed warning (fetal toxicity), hyperkalemia, contraindications (FDA label) — FDA / DailyMed
- Angiotensin II Receptor Blockers — mechanism, adverse effects, no-cough advantage — StatPearls (NCBI)
- DIOVAN (valsartan) — prescribing information — DailyMed (NLM)
- BENICAR (olmesartan) — prescribing information — DailyMed (NLM)
- ATACAND (candesartan) — prescribing information — DailyMed (NLM)
- Antihypertensives — ARBs / losartan (Ch. 6.10) — Open RN — Nursing Pharmacology
- The use of stems in the selection of INN (stem -sartan) — World Health Organization
- Antihypertensive Medications — ACE inhibitor/ARB monitoring, expected creatinine rise, contraindications, cough rates — StatPearls (NCBI)
- Hyperkalemia — RAAS inhibitors as a cause; life-threatening arrhythmias — StatPearls (NCBI)
- Lithium Toxicity — ARBs reduce lithium clearance — StatPearls (NCBI)
Reviewed by Hae Suk Lee, RN
Educational summary for nursing students. Always verify against current prescribing information and your institution's protocols before administering. Not medical advice.