Captopril is a medicine for high blood pressure and heart failure (ACE inhibitor). It is taken orally, preferably one hour before meals, because food reduces its absorption. It can cause a dry cough — a common effect of this class of medicines.
Also known as: Capoten
No clinically relevant adverse interaction. An ACE inhibitor plus a calcium-channel blocker is a first-line antihypertensive combination; additive hypotension is expected and only requires BP monitoring during titration. Not contraindicated.
An angiotensin-converting enzyme inhibitor (captopril) combined with a calcium-channel blocker (amlodipine) is a first-line combination in the treatment of hypertension, with complementary and synergistic antihypertensive effects. There is no clinically relevant adverse interaction; the only expected effect is additive hypotension, desirable in uncontrolled hypertension, which only requires blood pressure monitoring during titration. In elderly patients or those with orthostatic hypotension, start with low doses and titrate gradually.
No clinically relevant adverse interaction. First-line antihypertensive combination; monitor blood pressure during titration.
Usual and recommended combination. Start at low doses and titrate gradually; monitor blood pressure in the early weeks.
DailyMed/FDA (NIH/NLM) — approved Captopril label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a43a5373-ded9-4912-8c98-edaec8352836 ; approved Amlodipine label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=58a67272-c4c7-4e2c-85a5-9d39034d12c3
Dual RAAS blockade (ACE+ARB) with risk of hypotension, hyperkalaemia and renal decline.
Dual RAAS blockade with an ARB and an ACE inhibitor adds the effects on renal haemodynamics and potassium balance. The captopril label documents "Dual Blockade of the Renin-Angiotensin System (RAS)" as associated with "increased risks of hypotension, hyperkalaemia, and changes in renal function (including acute renal failure)" and recommends close monitoring of BP, renal function and electrolytes when the combination is unavoidable; the valsartan label states "Dual inhibition of the RAS: Increased risk of renal impairment, hypotension, and hyperkalemia". Major trials (ONTARGET, ALTITUDE) showed that dual blockade does not reduce mortality and increases renal adverse events and hyperkalaemia. Avoid in most hypertensive patients; consider only under specialist supervision in selected HF (Val-HeFT, PARADIGM-HF), with rigorous monitoring of BP, creatinine and potassium one week after initiation/adjustment and whenever therapy changes.
Valsartan + captopril: dual RAAS blockade — higher risk of hypotension, hyperkalaemia and renal impairment. Avoid in most patients.
Enhanced RAAS blockade removes renal compensation and raises potassium.
Potassium, creatinine, blood pressure.
Hypotension or hyperkalaemia.
Avoid routinely; if used, monitor potassium, creatinine and BP.
DailyMed (FDA) — approved Valsartan label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=1a8af3d9-4053-4233-82a7-e8c7bc9e302f ; approved Captopril label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=563737c5-4d63-4957-8022-e3bc3112dfac — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Combining Lithium with Captopril increases serum Lithium concentrations, with a risk of toxicity.
Angiotensin-converting enzyme (ACE) inhibitors such as captopril can raise serum lithium levels and cause signs of lithium toxicity in patients on concomitant lithium; the captopril label recommends co-administering with caution and monitoring serum lithium levels frequently, noting that if a diuretic is also used, the risk of lithium toxicity increases. Monitoring is especially important when starting the ACE inhibitor and at any dose change, and should include signs of lithium toxicity (tremor, confusion, ataxia, dysarthria, diarrhoea).
Captopril + lithium: the ACE inhibitor can raise lithium levels and cause toxicity. Use with caution and monitor lithium levels frequently.
Captopril, an angiotensin-converting enzyme inhibitor, reduces the renal excretion of Lithium, raising its levels.
Monitor Lithium levels after starting Captopril.
Signs of Lithium toxicity require discontinuation and evaluation.
Monitor Lithium levels and renal function during co-administration.
DailyMed/FDA (NIH/NLM) — approved Lithium label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=0e6b0a2d-b79c-44d8-b785-5267df9e8f72 ; approved Captopril label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a43a5373-ded9-4912-8c98-edaec8352836 — with additional reference: Prontuário Terapêutico do INFARMED, INFARMED (11th ed., 2012)
Food reduces captopril absorption by about 30-40%, lowering its bioavailability.
Take captopril one hour before meals.
EMC-UK (MHRA) — approved Captopril SmPC: https://www.medicines.org.uk/emc/product/5250/smpc
Captopril is contraindicated in previous ACE-inhibitor-associated angioedema.
Do not use in patients with a history of angioedema; use an alternative class.
EMC-UK (MHRA) — approved Captopril SmPC: https://www.medicines.org.uk/emc/product/5250/smpc
Captopril is contraindicated in pregnancy: ACE inhibitors may cause fetal renal injury, oligohydramnios and skull hypoplasia, especially in the 2nd and 3rd trimesters.
Do not start in pregnancy; if pregnancy is detected, stop captopril immediately.
Not recommended during breastfeeding; prefer an alternative with an established safety profile.
Women of childbearing age must use effective contraception during treatment.
EMC-UK (MHRA) — approved Captopril SmPC: https://www.medicines.org.uk/emc/product/5250/smpc
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Angiotensin-converting enzyme inhibitor (ACEI): reduces angiotensin II formation and increases bradykinin, lowering peripheral vascular resistance and blood pressure. In hypertension it usually does not change cardiac output; it increases renal blood flow. Blood pressure reduction is maximal 60–90 minutes after an oral dose; the effect is dose-dependent and may be progressive over weeks.
Captopril blocks the conversion of angiotensin I to angiotensin II (a potent vasoconstrictor and aldosterone stimulus) and reduces the degradation of bradykinin (a vasodilator). The antihypertensive effect of ACEIs adds to that of thiazide diuretics, but is less than additive with beta-blockers.
After oral administration, absorption is rapid, with peak blood levels at about one hour. Food reduces absorption by 30–40% — it should be given one hour before meals. Average minimal absorption is approximately 75%; 25–30% of the circulating drug is bound to plasma proteins.
Captopril is partially metabolised: in 24-hour urine, 40–50% is unchanged drug, and most of the remainder is the captopril disulfide dimer and captopril-cysteine disulfide. Over 95% of the absorbed dose is eliminated in the urine within 24 hours; retention occurs in renal impairment.
The apparent elimination half-life of unchanged drug is probably less than 2 hours (the half-life of total blood radioactivity is <3 hours). Retention occurs in renal impairment.
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
