Capoten, tablets 25 mg 56 pcs

Captopril is a highly specific competitive first generation angiotensin-converting enzyme (ACE) inhibitor containing a sulfhydryl group (SH-group). It reduces the activity of the renin-angiotensin-aldosterone system (RAAS). By inhibiting ACE, captopril reduces the conversion of angiotensin I to angiotensin II and eliminates the vasoconstrictor effect of the latter on arterial and venous vessels. As a result of decreasing the concentration of angiotensin II, there is a secondary increase in plasma renin activity (due to the elimination of negative feedback) and a decrease in aldosterone secretion by the adrenal cortex. The antihypertensive effect of captopril does not depend on the activity of plasma renin. Decrease of BP is noted with normal and even reduced activity of the hormone, which is due to the effect on tissue RAAS.

Captopril reduces ACE-mediated degradation of bradykinin and increases its content in body tissues. As a result of ACE inhibition, circulating and tissue kallikrein-kinin system activity increases, which contributes to peripheral vasodilation by accumulation of bradykinin (a peptide with a marked vasodilatory effect) and increased synthesis of prostaglandin E2. This mechanism may contribute to some antihypertensive effect of captopril, and is also the cause of some adverse reactions (in particular, dry cough).

In patients with arterial hypertension, captopril reduces blood pressure (BP) without a compensatory increase in heart rate (HR), fluid retention and sodium ions in the body. After a single oral administration, maximum antihypertensive effect is observed after 60-90 minutes. The degree of blood pressure reduction is the same when the patient is “standing” and “lying down”. Duration of the antihypertensive effect depends on the dose of the drug. The antihypertensive effect of captopril may increase over time and reaches optimal values after several weeks of therapy. Orthostatic hypotension rarely develops, mainly in patients with reduced circulating blood volume. Sudden discontinuation of captopril usually does not lead to development of “withdrawal” syndrome.

In patients with arterial hypertension, captopril increases renal blood flow while glomerular filtration rate is usually unchanged. With long-term use, it reduces left ventricular myocardial hypertrophy.

When captopril is taken sublingually in patients with uncomplicated hypertensive crisis, the onset of antihypertensive action is noted after 10-20 minutes; the maximum antihypertensive effect is seen after 45-60 minutes.

In patients with chronic heart failure (CHF), captopril significantly decreases total peripheral vascular resistance (TPV) and increases venous volume (thus reducing pre- and post-load on heart), decreases right atrial and small circulatory pressure, increases cardiac output and improves exercise tolerance.

In placebo-controlled clinical trials in patients with left ventricular dysfunction (left ventricular ejection fraction ≤40%) after myocardial infarction, captopril increased survival, delayed the development of clinically significant heart failure, and reduced rates of hospitalizations for heart failure.

In a clinical trial in patients with type I diabetes mellitus, diabetic nephropathy, retinopathy, and proteinuria ≥500 mg/day, captopril reduced proteinuria and reduced the rate of progression of diabetic nephropathy. The efficacy and safety of captopril in children have not been established.

Indications

Active ingredient

How to take, the dosage

Doses of Capoten should be selected by a doctor.

Internal, one hour before a meal, 25-50 mg 2-3 times daily (but no more than 450 mg per day), for children the initial dose is 0.15-0.3 mg/kg (but no more than 6 mg/kg per day).

Interaction

Diuretics, vasodilators, ganglioblocators, adrenoblockers when used simultaneously increase the antihypertensive effect of Capotene.

Indomethacin and other NSAIDs, as well as clonidine may decrease the antihypertensive effect of Capoten.

With simultaneous use of Capoten with allopurinol and procainamide, neutropenia and/or Stevens-Johnson syndrome may be observed, but the causal relationship of these phenomena is not clear.

The simultaneous use of immunosuppressants (e.g., azathioprine and cyclophosphamide) with Capoten increases the risk of hematological disorders.

Concomitant use of probenecid decreases urinary excretion of captopril.

The concomitant use of lithium salts and Capoten may increase the serum lithium concentration. This increases the risk of side effects and toxic effects of lithium preparations.

The simultaneous use of Capotene with potassium-saving diuretics (triamterene, amiloride and spironolactone) or potassium preparations may lead to hyperkalemia.

Special Instructions

Caution should be exercised when prescribing Capoten in collagenosis due to increased risk of neutropenia and agranulocytosis.
When prescribing the drug in patients with significant disorders of water-electrolyte balance, this condition should be corrected. During treatment with Capoten it is not recommended to take potassium-saving diuretics or potassium preparations, especially in patients with significant renal impairment.

The angioedema of the extremities, face, lips, mucous membranes, tongue, pharynx or larynx is observed in patients when using ACE inhibitors, including captopril. If the swelling is limited to the face and lips, this condition usually subsides after discontinuation of the drug. Antihistamines may be used to relieve clinical symptoms. Patients should be monitored by a physician until symptoms disappear. If the swelling involves the tongue, pharynx or larynx with risk of airway obstruction, 0.5 ml of 0.1% adrenaline solution should be injected intravenously.

A low-sodium diet is indicated during treatment with Capoten.

Capotene may cause a false-positive urine test for acetone.

Pediatric use

The safety and effectiveness in children have not been studied.

Contraindications

Hypersensitivity in history (including history of other ACE inhibitors). to other ACE inhibitors), Quincke’s edema (hereditary or associated with a history of ACE inhibitors use), marked renal and hepatic dysfunction, hyperkalemia, bilateral renal artery stenosis or stenosis of the artery of the sole kidney with progressive azotemia, conditions after renal transplantation, aortic stenosis and similar obstructive changes impeding blood flow, pregnancy, breast-feeding period.

Side effects

Cardiovascular system: orthostatic hypotension, tachycardia, peripheral edema.

Respiratory system: dry cough, bronchospasm, pulmonary edema.

Allergic reactions: angioedema of the extremities, face, lips, mucous membranes, tongue, pharynx or larynx.

Water-electrolyte balance: hyperkalemia (most likely in renal failure), hyponatremia (most often in salt-free diet and concomitant use of diuretics.

Urinary system disorders: proteinuria, increased plasma urea nitrogen and creatinine, acidosis.

Hematopoietic system disorders: in rare cases – neutropenia, agranulocytosis, thrombocytopenia and anemia, positive test for antibodies to nuclear antigen. In patients with normal renal function (CK less than 1.6 mg/dL) in the absence of other complicating factors, neutropenia was observed in 0.02% of cases.

Digestive system disorders: reversible and usually self-liquidating taste disorder, dry mouth, aphthous stomatitis; rarely – abdominal pain, diarrhea, gum hyperplasia, hepatitis, increased level of liver plasma transaminases, hyperbilirubinemia.

Dermatological reactions: maculopapular rash, usually accompanied by itching and in rare cases – by increase in body temperature; hyperemia, vesicular or bullous rash, erythema (including Stevens-Johnson syndrome), photosensitization.

CNS and peripheral nervous system disorders: headache, dizziness, ataxia, paresthesia, somnolence, visual disorders.

Overdose

Symptoms: marked decrease in BP.

Treatment: administration of plasma substitute drugs and hemodialysis are effective.

Similarities