Lisinopril Stada, tablets 10 mg 20 pcs

Lisinopril is cardioprotective, natriuretic, vasodilatory, hypotensive.

Pharmacodynamics

A ACE inhibitor, reduces the formation of angiotensin II from angiotensin I.

The decrease in angiotensin II leads to a direct decrease in aldosterone release.

Decreases bradykinin degradation and increases prostaglandin synthesis.

Limits total peripheral vascular resistance, blood pressure (BP), preload, pulmonary capillary pressure, causes an increase in the minute blood volume and increases myocardial exercise tolerance in patients with chronic heart failure.

Dilates arteries to a greater extent than veins. Some effects are explained by the effect on tissue renin-angiotensin systems.

Long-term use reduces myocardial hypertrophy and arterial resistive walls. It improves the blood supply to the ischemic myocardium.

The ACE inhibitors prolong life expectancy in patients with chronic heart failure and slow the progression of left ventricular dysfunction in patients who have had myocardial infarction without clinical manifestations of heart failure.

The antihypertensive effect begins after approximately 6 hours and lasts for 24 hours. The duration of the effect also depends on the dose.

The onset of action is after 1 h. The maximum effect is determined after 6-7 hours. In case of arterial hypertension, the effect is noted in the first days after the start of treatment, the stable effect develops after 1-2 months.

When the drug is abruptly withdrawn, no pronounced increase in BP has been observed.

In addition to lowering BP, lisinopril decreases albuminuria. In patients with hyperglycemia, it helps to normalize the function of the damaged glomerular endothelium.

Lisinopril has no effect on blood glucose concentration in diabetic patients and does not lead to increased incidence of hypoglycemia.

Pharmacokinetics

Intake. After oral administration, approximately 25% of lisinopril is absorbed from the gastrointestinal tract.

Eating does not affect absorption of the drug. Absorption is on average 30% and bioavailability is 29%.

Distribution. Almost does not bind with blood plasma proteins. Maximal concentration in blood plasma (90 ng/ml) is reached after 7 hours.

Permeability through the blood-brain barrier and the placental barrier is low.

Metabolism. Lisinopril is not biotransformed in the body.

Elimination. It is excreted unchanged by the kidneys. The elimination half-life is 12 hours.

Pharmacokinetics in selected patient groups

In patients with chronic heart failure the absorption and clearance of lisinopril are decreased.

In patients with renal failure, lisinopril concentrations are several times higher than plasma concentrations in volunteers, with increased time to peak plasma concentrations and increased elimination half-life.

In elderly patients the plasma concentration of the drug and area under the curve are 2 times higher than in younger patients.

Indications

Active ingredient

Composition

How to take, the dosage

Interaction

Special Instructions

Contraindications

Side effects

Overdose

Pregnancy use

The use of lisinopril during pregnancy is contraindicated. If pregnancy is established, the drug should be discontinued as soon as possible.

The use of ACE inhibitors in the second and third trimesters of pregnancy has adverse effects on the fetus (marked BP decrease, renal failure, hyperkalemia, skull hypoplasia, fetal death are possible).

There are no data about negative effect of the drug on the fetus in case of its use during the first trimester.

In newborns and infants who have had intrauterine exposure to ACE inhibitors are recommended to be closely monitored for timely detection of marked BP decrease, oliguria, hyperkalemia.

Lisinopril penetrates through the placenta. There are no data on permeation of Lisinopril into breast milk. Breastfeeding should be stopped during treatment with the drug.

Similarities