Treatment of arterial hypertension. Treatment of clinically expressed heart failure. Prevention of clinically expressed heart failure in patients with asymptomatic left ventricular dysfunction (ejection fraction ≤ 35%).
Enap 2.5 mg. Storage
active substance: enalapril maleate;
1 tablet contains 2.5 mg or 5 mg, or 10 mg, or 20 mg of enalapril maleate;
Enap 2.5 mg. Excipients: tablets of 2.5 mg and 5 mg: sodium bicarbonate, lactose monohydrate, corn starch, hydroxypropylcellulose, talc, magnesium stearate;
10 mg and 20 mg tablets: sodium bicarbonate, lactose monohydrate, corn starch, talc, magnesium stearate, iron oxide red (E 172), iron oxide yellow (E 172) – only for tablets of 20 mg.
Enap 2.5 mg. Dosage form
Basic physical and chemical properties:
2.5 mg tablets: round biconvex white tablets with a beveled edge;
5 mg tablets: round flat tablets of white color with a beveled edge and a notch on one side;
10 mg tablets: round flat reddish-brown tablets with a beveled edge and a notch on one side, with white patches on the surface and in the weight of the tablet;
20 mg tablets: round, light orange tablets with a beveled edge and a notch on one side, with white patches on the surface and weight of the tablet.
Agents acting on the renin-angiotensin system. Angiotensin-converting enzyme inhibitors. ATX code C09A A02.
Enalapril maleate is a salt of maleic acid and enalapril, a derivative of two amino acids – L-alanine and L-proline.
Mechanism of action
Angiotensin converting enzyme (ACE) is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the pressor substance angiotensin II. After absorption, enalapril is hydrolyzed to enalaprilat, which inhibits ACE inhibitors. ACE inhibition causes a decrease in plasma angiotensin II levels, leading to increased plasma renin activity (due to suppression of the negative feedback between angiotensin II activity and renin release) and decreased aldosterone secretion.
ACE is identical to kininase II. Thus, enalapril can also block the cleavage of bradykinin, a strong vasodepressor peptide. However, the significance of this phenomenon for the therapeutic effect of the drug remains unclear.
The mechanism by which enalapril lowers blood pressure is primarily associated with inhibition of the activity of the renin-angiotensin-aldosterone system (RAAS). Enalapril may have an antihypertensive effect even in patients with low-renin hypertension.
The use of Enap® in the case of hypertension causes a decrease in blood pressure in patients in horizontal and vertical positions without a significant increase in heart rate.
Symptomatic postural hypotension occurs infrequently. In some patients, achieving optimal blood pressure reduction may require several weeks of therapy. Sudden withdrawal of Enap® was not associated with a rapid increase in blood pressure.
Treatment of arterial hypertension.
Treatment of clinically severe heart failure.
Prevention of clinically severe heart failure in patients with asymptomatic left ventricular dysfunction (ejection fraction ≤ 35%).
Hypersensitivity to enalapril or to any of the other ingredients, or to other ACE inhibitors.
History of angioneurotic edema associated with prior ACE inhibitor therapy.
Hereditary or idiopathic angioneurotic edema.
Pregnancy or pregnancy planning (see section “Use during pregnancy or breastfeeding”).
Enap® should not be used with aliskiren-containing products in patients with diabetes mellitus or renal impairment (GFR <60 ml / min / 1.73 m2).
Concomitant use in combination with neprilysin inhibitors (eg sacubitrile) – due to an increased risk of angioneurotic edema. The drug should not be used within 36 hours after the last dose of sacubitril / valsartan – a drug containing a neprilysin inhibitor, or after switching from it to another drug (see sections “Specifics” and “Interaction with other medicinal products and other forms of interaction”) .