ARBs

High-yield Verified · Jul 2026

Prototype: losartan

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.

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ARBs block the AT₁ receptor rather than the enzyme — so bradykinin is not affected (no cough).

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 (up to ~10% of patients) and, rarely, angioedema. Because ARBs act at the receptor and leave ACE — and therefore bradykinin — untouched, they do not 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

Generic Brand

losartan Cozaar

valsartan Diovan

olmesartan Benicar

candesartan Atacand

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 no cough).

In plain terms

They stop angiotensin II from doing its job at the receptor, so blood vessels relax and blood pressure falls — without the ACE-inhibitor cough.

Therapeutic effects — what you'll see working

The effects — and how you judge them — mirror ACE inhibitors: a gradual blood-pressure fall over 1–2 weeks, plus protective benefit in heart failure and diabetic kidney disease. Reserve them especially for the ACE-intolerant patient.

↓ Blood pressure Renal protection No dry cough

↓ 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 (with the same expected small creatinine rise as ACE inhibitors).
No dry cough: Because bradykinin is not affected, ARBs avoid the ACE-inhibitor cough — the main 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) — minus the bradykinin problems.

Common Hold & notify

Hyperkalemia, dizziness, first-dose/orthostatic hypotension, mildly rising serum creatinine.

Hyperkalemia arises because low aldosterone makes the kidney retain potassium — the risk climbs with potassium supplements, salt substitutes, kidney disease, or combination with an ACE inhibitor. A small creatinine rise is expected and reflects the intended drop in glomerular pressure.

Serious Report immediately

Angioedema (rare — much less than ACE inhibitors), acute kidney injury (bilateral renal artery stenosis), severe hyperkalemia.

Angioedema is rare with ARBs but can still occur — do not assume the class is immune, especially in a patient who had it on an ACE inhibitor. Acute kidney injury happens when the kidney depended on angiotensin II to maintain filtration (bilateral renal artery stenosis).

■ Boxed warning · fetal toxicity

Can cause fetal injury and death — discontinue as soon as pregnancy is detected.

In the 2nd and 3rd trimesters, blocking the fetal RAAS impairs kidney development and urine output, causing oligohydramnios, lung/skull underdevelopment, renal failure, and death. Any patient of childbearing potential must understand this before starting.

Interactions

K-sparing diuretics, potassium supplements, salt substitutes drug

Additive potassium retention → potentially fatal hyperkalemia.

NSAIDs drug

Blunt the antihypertensive effect and add renal risk (↓ effect / renal impairment).

Lithium drug

Reduced lithium clearance → ↑ lithium levels and toxicity.

Contraindications

The contraindications match ACE inhibitors — situations where removing angiotensin II effect is dangerous — because the end target is the same.

Pregnancy

Fetal renal toxicity, oligohydramnios, and death (the boxed warning). Stop immediately if pregnancy occurs.

Concurrent aliskiren in diabetes; generally avoid combining with an ACE inhibitor

Dual RAAS blockade sharply increases hyperkalemia, hypotension, and renal failure without added benefit.

Bilateral renal artery stenosis

These kidneys depend on angiotensin II to maintain filtration pressure — blocking it precipitates acute kidney injury.

History of angioedema; hyperkalemia use caution

Angioedema can recur, and ARBs raise potassium — starting one with an already-high level risks dangerous arrhythmias.

When to hold

Assess before giving — these findings mean hold the dose and act.

Pregnancy (boxed warning — contraindicated)

Stop the drug immediately — fetal renal toxicity, oligohydramnios, and death.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Monitoring

Check potassium and creatinine at baseline and after dose changes.

Why: Falling aldosterone raises potassium and lower glomerular pressure raises creatinine; a mild creatinine bump is acceptable, but a large rise or hyperkalemia signals kidney compromise.

Monitor blood pressure and watch for first-dose hypotension, especially in volume-depleted or diuretic-treated patients.

Why: Removing angiotensin II support can drop BP, causing dizziness or falls early in therapy.

Patient teaching

Do not use if pregnant or planning pregnancy; use reliable contraception.

Why: Fetal toxicity is the boxed warning, greatest in the 2nd and 3rd trimesters.

Avoid potassium-based salt substitutes and potassium supplements unless told otherwise; report facial/lip swelling.

Why: These add to the drug’s potassium-raising effect; swelling could signal rare angioedema.

Rise slowly from sitting or lying, and keep follow-up lab appointments.

Why: Orthostatic hypotension is common early, and potassium/creatinine must be tracked over time.

Sources

Educational summary for nursing students. Always verify against current prescribing information and your institution's protocols before administering. Not medical advice.