Losartan
Is It Right for You?
A complete guide to Losartan — what it treats, how it works, dosages, side effects, and when a clinician may prescribe it following an online consultation.
What Is Losartan?
Losartan is an orally administered angiotensin II receptor blocker (ARB) — also known as an angiotensin receptor antagonist (ARA) or sartans — used primarily for the treatment of hypertension, heart failure, and diabetic nephropathy. It was the first ARB to receive regulatory approval globally, introduced in 1995, and remains one of the most widely prescribed antihypertensive agents worldwide.
Losartan selectively and competitively blocks the angiotensin II type 1 (AT1) receptor — the primary receptor through which angiotensin II exerts its vasoconstrictive, sodium-retaining, and aldosterone-stimulating effects. By blocking this receptor, losartan reduces blood pressure, decreases cardiac afterload, and provides organ-protective effects in the kidneys and cardiovascular system. It is available generically and in the combination product Cozaar (losartan alone) and Cozaar-Comp / Hyzaar (losartan with hydrochlorothiazide). Tablets are available in 12.5 mg, 25 mg, 50 mg, and 100 mg formulations.
What Conditions Does Losartan Treat?
Losartan is prescribed for:
Renin-angiotensin-aldosterone system (RAAS) blockade is central to the management of heart failure with reduced ejection fraction. Losartan is used as an alternative to ACE inhibitors in patients who cannot tolerate ACE inhibitors due to cough or angioedema. The HEAAL trial demonstrated that higher-dose losartan (150 mg daily) produced greater reductions in heart failure hospitalisations and death compared with standard doses. Losartan is not recommended for concurrent use with an ACE inhibitor (dual RAAS blockade) due to increased risk of adverse effects including hyperkalaemia and acute kidney injury.
Losartan has a specific licensed indication for renoprotection in patients with type 2 diabetes and nephropathy (kidney disease with proteinuria). The RENAAL trial demonstrated that losartan significantly reduced the rate of progression to end-stage renal disease, doubling of serum creatinine, and the composite endpoint of renal outcomes in this population, over and above its blood pressure-lowering effect. This renoprotective benefit is mediated by reducing intraglomerular pressure and proteinuria.
The LIFE trial demonstrated that losartan was superior to atenolol (a beta-blocker) in reducing the risk of stroke in hypertensive patients with left ventricular hypertrophy (LVH), a finding that established ARBs as preferred antihypertensives in this population.
While Losartan is effective for managing hypertension and heart failure, it should be used cautiously in patients with a history of hypersensitivity or renal impairment.
How Does Losartan Work?
Angiotensin II is the principal effector hormone of the renin-angiotensin-aldosterone system (RAAS). It is generated when renin (released from the kidney in response to low blood pressure, low sodium, or sympathetic activation) cleaves angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II exerts its biological effects predominantly through the AT1 receptor, causing: potent vasoconstriction of systemic arterioles (raising blood pressure), sodium and water retention via aldosterone stimulation, increased sympathetic nervous system activity, thirst stimulation, and promotion of cardiac and vascular hypertrophy and renal fibrosis.
Losartan selectively and competitively blocks the AT1 receptor, preventing angiotensin II from binding and activating it. This produces: vasodilation (reducing peripheral vascular resistance and blood pressure), natriuresis (increased sodium and water excretion), reduced aldosterone secretion (reducing sodium retention and potassium loss), and regression of pathological cardiac, vascular, and renal changes driven by chronic angiotensin II stimulation. Unlike ACE inhibitors, ARBs do not inhibit the breakdown of bradykinin — a peptide whose accumulation is responsible for the dry, persistent cough that affects approximately 10–15% of ACE inhibitor users and is the most common reason for switching to an ARB.
Losartan has the additional property of being uricosuric — it mildly reduces serum uric acid levels by inhibiting urate reabsorption in the kidney. This is clinically relevant in hypertensive patients with gout or hyperuricaemia, in whom losartan may be the preferred ARB.
Dosages & Administration
The correct dose depends on the type and severity of infection, age, weight, and kidney function. Always follow your clinician's instructions. The table below is for general reference only.
Administration Tips
Losartan tablets may be taken at any time of day, with or without food. Taking at the same time daily improves adherence. Tablets should be swallowed whole with water. There is no requirement for dose titration for standard hypertension; the 50 mg starting dose is typically appropriate for most adults with normal renal function.
Side Effects of Losartan
Losartan is generally well tolerated, but some side effects may occur.
- Dizziness and hypotension: Particularly at initiation or dose increase; more pronounced in patients who are volume-depleted, on diuretics, or have heart failure. First-dose hypotension is less dramatic than with ACE inhibitors but can occur.
- Hyperkalaemia (elevated potassium): Due to reduced aldosterone-mediated potassium excretion; risk increased with renal impairment, diabetes, and concurrent use of potassium-sparing diuretics or potassium supplements.
- Elevated creatinine: A modest rise in serum creatinine (up to 30% from baseline) is expected and acceptable when initiating ARBs, reflecting the intended reduction in intraglomerular pressure. A rise exceeding 30% or a sharp acute rise warrants urgent review.
- Headache, fatigue
- Upper respiratory tract symptoms: Including nasal congestion
- Angioedema: Significantly less common than with ACE inhibitors, but not absent — cases of losartan-associated angioedema have been reported. Patients who have had ACE inhibitor-induced angioedema have a small but non-negligible risk of ARB-associated angioedema. Angioedema of the tongue, lips, or throat is a medical emergency.
- Acute kidney injury: In patients with bilateral renal artery stenosis, severe heart failure, or significant volume depletion, RAAS blockade can precipitate acute renal failure by removing the angiotensin II-dependent maintenance of glomerular filtration pressure.
- Hepatotoxicity: Very rare; monitor liver function if hepatic symptoms develop.
Patients should be informed about the risk of angioedema and the importance of seeking emergency care if they experience swelling.
Drug Interactions
Inform your clinician about all medications you are taking, as some drugs may interact with Losartan and affect its efficacy.
Additive effects may cause significant hyperkalemia (high potassium levels), which can lead to cardiac arrhythmias. Avoid routine combination unless closely monitored.
Concurrent use increases risk of hypotension, hyperkalemia, and kidney impairment. Dual RAAS blockade should generally be avoided unless under specialist supervision.
NSAIDs may reduce antihypertensive effectiveness and increase the risk of kidney impairment, especially in elderly or dehydrated patients. Monitor renal function and blood pressure.
May enhance hypotensive effect, especially when starting lisinopril, increasing risk of dizziness or fainting. Monitor blood pressure during initiation.
Important Warnings
Do not take losartan during pregnancy. It can cause serious harm or death to the developing baby, particularly from the second trimester. Use effective contraception while on treatment and switch to a safer antihypertensive as soon as pregnancy is planned or confirmed.
Seek emergency medical attention immediately if you develop swelling of the face, lips, tongue, or throat while taking losartan. Although less common than with ACE inhibitors, ARB-associated angioedema is a life-threatening emergency.
Regular use of ibuprofen, naproxen, or other NSAIDs while taking losartan significantly increases the risk of kidney injury, particularly in the elderly or those with pre-existing kidney disease. Use paracetamol for pain relief instead.
Many over-the-counter "low sodium" salt substitutes contain high amounts of potassium chloride. These can cause dangerous hyperkalaemia in patients taking ARBs. Avoid unless specifically advised by a clinician.
Speak to a Clinician About Treatment
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The treatment you need, when you need it.
Losartan FAQs
The most common reason for switching from an ACE inhibitor (such as ramipril or lisinopril) to an ARB (such as losartan) is ACE inhibitor-induced cough — a dry, persistent, irritating cough caused by bradykinin accumulation that affects approximately 10–15% of patients taking ACE inhibitors. Because ARBs block the renin-angiotensin system at a different point and do not affect bradykinin levels, they do not cause this cough. Both classes provide equivalent blood pressure reduction and organ protection for most indications.
Losartan has a dual effect on kidney function. In the short term, it causes a modest, expected rise in serum creatinine by reducing intraglomerular pressure — this is monitored with blood tests. In the long term, this reduction in intraglomerular pressure is protective, slowing the progression of CKD and proteinuria, particularly in patients with diabetes. Regular blood monitoring of renal function and electrolytes is therefore important both for safety and to confirm long-term benefit.
Regular or high-dose ibuprofen (and other NSAIDs) should be avoided with losartan. NSAIDs reduce renal blood flow and can cause acute kidney injury in patients already dependent on angiotensin II for maintaining glomerular filtration (particularly elderly patients, those with CKD, or those on diuretics). NSAIDs also blunt the antihypertensive effect of losartan. Paracetamol is a safer analgesic option in patients taking ARBs.
Losartan has a mild uricosuric effect — it increases urinary uric acid excretion, modestly reducing serum uric acid levels. This makes it the preferred ARB (and one of the preferred antihypertensives overall) in hypertensive patients with gout or hyperuricaemia, as many other antihypertensives (particularly thiazide diuretics and beta-blockers) raise uric acid levels and can precipitate gout attacks.
Yes. Renal function (creatinine, eGFR) and electrolytes (particularly potassium) should be checked before starting losartan, 1–2 weeks after initiation or any dose change, and then at least annually once stable. More frequent monitoring is required in patients with CKD, heart failure, or concurrent use of other medications affecting potassium or renal function.
