ACE inhibitor. The mechanism of antihypertensive action is associated with inhibition of ACE activity, which leads to a decrease in the rate of conversion of angiotensin I to angiotensin II (which has a pronounced vasoconstrictor effect and stimulates the secretion of aldosterone in the adrenal cortex). As a result of a decrease in the formation of angiotensin II, a secondary increase in plasma renin activity occurs due to the elimination of negative feedback during renin release and a direct decrease in aldosterone secretion. A decrease in aldosterone secretion may contribute to an increase in potassium concentration. Lisinopril reduces OPSS, reduces blood pressure, preload, pressure in the pulmonary capillaries, causes an increase in minute blood volume and increased myocardial exercise tolerance in patients with chronic heart failure (CHF). Expands arteries to a greater extent than veins. Some effects are explained by the effect on tissue renin-angiotensin-aldosterone systems (RAAS). With prolonged use, this leads to the reverse development of myocardial hypertrophy and pathological remodeling in the cardiovascular system. Improves endothelial function and blood supply to the ischemic myocardium. ACE inhibitors lengthen life expectancy in patients with heart failure, slow the progression of left ventricular dysfunction in patients after myocardial infarction without clinical manifestations of heart failure. Lisinopril reduces albuminuria. In patients with hyperglycemia, it helps normalize the function of damaged glomerular endothelium. It does not affect the blood glucose concentration in patients with diabetes mellitus and does not lead to an increase in cases of hypoglycemia.


After oral administration, lisinopril is slowly and incompletely absorbed from the digestive tract. Absorption is on average 25%, characterized by high variability - 6-60%. Bioavailability is 29%. Plasma Cmax is reached after approximately 7 hours. Plasma protein binding is negligible. It is excreted unchanged in urine. In patients with normal renal function, T1 / 2 is 12 hours. Lisinopril is excreted during hemodialysis.


Hypersensitivity to lisinopril, other ACE inhibitors; history of angioedema, including against the background of the use of ACE inhibitors; hereditary Quincke edema or idiopathic angioedema; pregnancy; period of breastfeeding; age up to 18 years (effectiveness and safety have not been established); hemodialysis or hemofiltration using high-flow high-permeability dialysis membranes (e.g. AN69); apheresis of low density lipoproteins using dextran sulfate; desensitizing therapy to the poison of Hymenoptera insects (bees, wasps); simultaneous use with aliskiren and drugs containing aliskiren in patients with diabetes mellitus and / or moderate or severe impaired renal function (CC less than 60 ml / min); simultaneous use with angiotensin II receptor antagonists (ARA II) in patients with diabetic nephropathy. With caution: impaired renal function; bilateral renal artery stenosis or artery stenosis of a single kidney; condition after kidney transplantation; azotemia; hyperkalemia aortic stenosis, mitral stenosis; hypertrophic obstructive cardiomyopathy; primary hyperaldosteronism; arterial hypotension; cerebrovascular disease (including cerebrovascular insufficiency); Ischemic heart disease; coronary insufficiency, autoimmune systemic diseases of the connective tissue (including systemic lupus erythematosus, scleroderma); inhibition of bone marrow hematopoiesis; hypovolemic conditions (including as a result of diarrhea, vomiting); salt restriction diet; advanced age (over 65 years old); use in patients of the black race; simultaneous use with drugs containing aliskiren or angiotensin II receptor antagonists (with double blockade of RAAS, there is an increased risk of developing arterial hypotension, hyperkalemia, and renal failure); diabetes.

Pregnancy and lactation

Contraindicated in pregnancy and lactation (breastfeeding). If necessary, use during lactation should decide on the termination of breastfeeding.

Side effects

From the hemopoietic system: rarely - a decrease in hemoglobin, a decrease in hematocrit; very rarely - inhibition of bone marrow function, anemia, thrombocytopenia, leukopenia, neutropenia, agranulocytosis, hemolytic anemia, lymphadenopathy. From the side of the immune system: infrequently - angioedema (face, lips, tongue, larynx or epiglottis, upper and lower limbs); rarely - a syndrome that includes an increase in ESR, arthralgia and the appearance of antinuclear antibodies, urticaria; very rarely - autoimmune diseases, intestinal neurotic edema. From the endocrine system: rarely - a syndrome of impaired secretion of antidiuretic hormone (ADH). From the psyche: infrequently - lability of mood; rarely anorexia; frequency is unknown - depression, confusion. From the nervous system: often - dizziness, headache; infrequently - paresthesia, sleep disturbance (drowsiness / insomnia); rarely - confusion, unknown frequency - convulsive twitching of the muscles of the limbs and lips. From the side of the organ of vision: rarely - visual impairment. On the part of the organ of hearing and labyrinth disorders: infrequently - vertigo. From the cardiovascular system: often - orthostatic hypotension; infrequently - a marked decrease in blood pressure, acute myocardial infarction, tachycardia, a feeling of palpitations; rarely - aggravation of the severity of symptoms and course of heart failure, impaired AV conduction, chest pain, cerebrovascular accident in patients at ""high risk"" due to a marked decrease in blood pressure, Raynaud's syndrome, vasculitis. From the respiratory system: often - dry cough; infrequently - rhinitis; very rarely - sinusitis, dyspnea, bronchospasm, allergic alveolitis / eosinophilic pneumonia. From the digestive system: often - nausea, vomiting, diarrhea; rarely - dry mouth, dyspepsia, abdominal pain, taste changes; very rarely - pancreatitis. From the liver and biliary tract: rarely - hepatocellular or cholestatic jaundice, hepatitis. From the urinary system: often - impaired renal function; rarely - uremia, acute renal failure; very rarely - oliguria, anuria; frequency unknown - proteinuria. On the part of the skin and subcutaneous tissues: infrequently - itching, rash, rarely - psoriasis, very rarely - pemphigus, toxic epidermal necrolysis (Dyel's syndrome), erythema multiforme, Stevens-Johnson syndrome, pseudolymphoma of the skin. From the musculoskeletal system: rarely - myalgia, arthralgia / arthritis. From the genitals and mammary gland: infrequently - sexual dysfunction, rarely - gynecomastia. On the part of laboratory indicators: infrequently - an increase in the concentration of urea in the blood plasma, hypercreatininemia, hyperkalemia, an increase in the activity of hepatic ""transaminases, rarely - hyperbilirubinemia, hyponatremia, very rarely - an increase in ESR, an increase in the titer of antinuclear antibodies, a decrease in glucose concentration. General reactions: rarely - fever, asthenia, increased fatigue, alopecia, impaired fetal development, very rarely - increased sweating.


With simultaneous use with antihypertensive agents, an additive antihypertensive effect is possible. With simultaneous use with potassium-sparing diuretics (spironolactone, triamteren, amiloride), potassium preparations, salt substitutes containing potassium, the risk of hyperkalemia increases, especially in patients with impaired renal function. With the simultaneous use of ACE inhibitors and NSAIDs, the risk of developing renal dysfunction increases, hyperkalemia is rarely observed. With simultaneous use with ""loop"" diuretics, thiazide diuretics, the antihypertensive effect is enhanced. The occurrence of severe arterial hypotension, especially after taking the first dose of a diuretic, apparently occurs due to hypovolemia, which leads to a transient increase in the hypotensive effect of lisinopril. Increased risk of impaired renal function. With simultaneous use with indomethacin, the antihypertensive effect of lisinopril decreases, apparently due to the inhibition of prostaglandin synthesis under the influence of NSAIDs (which are believed to play a role in the development of the hypotensive effect of ACE inhibitors). With simultaneous use with insulin, hypoglycemic agents, sulfonylurea derivatives, hypoglycemia may develop due to increased glucose tolerance. With simultaneous use with clozapine, the concentration of clozapine in blood plasma increases. With simultaneous use with lithium carbonate, the concentration of lithium in blood serum increases, accompanied by symptoms of lithium intoxication. Lisinopril slows the elimination of lithium preparations, which may increase the risk of side effects. Therefore, when used together, it is necessary to regularly monitor the lithium content in the blood plasma. A case of the development of severe hyperkalemia in a patient with diabetes mellitus with simultaneous use with lovastatin is described. The simultaneous use of lisinopril with beta-blockers, “slow” calcium channel blockers, diuretics, tricyclic antidepressants / antipsychotics and other antihypertensive drugs increases the severity of the hypotensive effect. Antacids and colestyramine reduce the absorption of lisinopril in the digestive tract. When combined with insulin and hypoglycemic agents for oral administration, the risk of developing hypoglycemia increases. With simultaneous use with NSAIDs, cyclooxygenase-2 inhibitors and acetylsalicylic acid (at a dose of more than 3 g / day), estrogens, sympathomimetics, the hypotensive effect of lisinopril is reduced. NSAIDs and ACE inhibitors increase plasma potassium and can impair renal function. This effect is usually reversible. The use of lisinopril in combination with acetylsalicylic acid as an antiplatelet agent, thrombolytic and / or nitrates is not contraindicated. With the simultaneous use of ethanol enhances the effect of lisinopril. With the simultaneous use of ACE inhibitors and gold preparations for iv administration (sodium aurothiomalate), a symptom complex has been described, including facial flushing, nausea, vomiting, and a decrease in blood pressure. The combined use with selective serotonin reuptake inhibitors can lead to severe hyponatremia. The combined use with allopurinol, procainamide, cytostatics may increase the risk of developing leukopenia. With simultaneous use with aliskiren and aliskiren-containing drugs in patients with diabetes mellitus and patients with impaired renal function of moderate and / or severe severity (CC less than 60 ml / min), the risk of hyperkalemia, impaired renal function and an increase in the frequency of cardiovascular morbidity and mortality. In elderly patients and patients with impaired renal function, concomitant use of ACE inhibitors with sulfamethoxazole / trimethoprim was accompanied by severe hyperkalemia, which is believed to be caused by trimethoprim, therefore, the drug should be used with caution with preparations containing trimethoprim, regularly monitoring the level of potassium in the blood plasma.

Dosage and administration

The method of application and the dosage regimen of a particular drug depends on its form of release and other factors. The optimal dosage regimen is determined by the doctor. The compliance of the dosage form of a particular preparation with the indications for use and the dosage regimen should be strictly observed. Set individually, depending on the indications, treatment regimen, kidney function. The initial dose of 2.5 mg 1 time / day. Maintenance doses of 5-20 mg.

Special instructions

Most often, a pronounced decrease in blood pressure occurs with a decrease in BCC caused by diuretic therapy, a decrease in salt intake, dialysis, diarrhea or vomiting. In patients with chronic heart failure with simultaneous renal failure or without it, a marked decrease in blood pressure is possible. In patients with coronary heart disease, cerebrovascular insufficiency, in whom a sharp decrease in blood pressure can lead to myocardial infarction or stroke, lisinopril should be prescribed only under strict medical supervision. Transient arterial hypotension is not a contraindication for taking the next dose of lisinopril. When using lisinopril in some patients with heart failure, but with normal or low blood pressure, a decrease in blood pressure may occur, which is usually not a reason for stopping treatment. In heart failure, severe arterial hypotension may result in impaired renal function. In some cases, in the presence of heart failure with normal or low blood pressure, lisinopril can also cause an additional decrease in blood pressure. This effect is not a contraindication for further administration of lisinopril. In patients with bilateral renal artery stenosis or stenosis of a single kidney artery, when treated with ACE inhibitors, in some cases, an increase in the concentration of urea nitrogen in blood plasma and serum creatinine was observed. These changes were almost always reversible and disappeared after the withdrawal of an ACE inhibitor. These complications are especially characteristic for patients with existing impaired renal function. If the patient has renovascular hypertension, then the risk of developing severe arterial hypotension and renal failure increases. In this category of patients, treatment should begin with lower doses of lisinopril under medical supervision. Since the simultaneous use of diuretics is an additional risk factor for the development of arterial hypotension, they should be abolished and kidney function monitoring should be carried out during the first week. An increase in the concentration of urea nitrogen in blood plasma and serum creatinine was also noted in patients with arterial hypertension without concomitant renal impairment, especially with the simultaneous use of lisinopril and diuretics. These changes were of mild severity, and the indicators returned to normal after discontinuation of lisinopril or diuretic. In patients with acute myocardial infarction, lisinopril therapy should not be started if there are signs of impaired renal function, expressed in an increase in plasma KK above 177 μmol / L and / or proteinuria above 500 mg / day. If impaired renal function develops while taking lisinopril (CC in the blood plasma is higher than 265 μmol / L or doubles compared to the values ​​before treatment), then it is necessary to consider the possibility of discontinuing lisinopril. Treatment with lisinopril in acute myocardial infarction is carried out against the background of standard therapy (thrombolytics, acetylsalicylic acid (as an antiplatelet agent), beta-blockers). Lisinopril can be used with a solution of nitroglycerin for iv administration or with the use of nitroglycerin sublingually. The use of lisinopril in patients after acute myocardial infarction is not recommended if the systolic blood pressure does not exceed 100 mm Hg. When using drugs that reduce blood pressure in patients with extensive surgery or during general anesthesia, lisinopril can block the formation of angiotensin II, secondary to compensatory renin secretion. Before surgery (including dental surgery), you should stop taking lisinopril for 24 hours and inform the surgeon / anesthetist about the use of an ACE inhibitor. It is suggested that the simultaneous administration of ACE inhibitors and insulin, as well as hypoglycemic drugs for oral administration, can lead to the development of hypoglycemia. The greatest risk of development is observed during the first weeks of combination therapy, as well as in patients with impaired renal function. Patients with diabetes require careful glycemic control, especially during the first month of treatment with an ACE inhibitor. Before starting treatment, it is necessary to compensate for the loss of fluid and salts. In patients with risk factors for the development of symptomatic arterial hypertension (patients on a diet with a limited intake of sodium chloride with or without hyponatremia, patients with hypovolemia or receiving diuretic therapy), these conditions should be adjusted if possible before treatment with lisinopril. Risk factors for the development of hyperkalemia include chronic renal failure, diabetes mellitus and the simultaneous use of potassium-sparing diuretics (spironolactone, eplerenone, triamteren, or amiloride), potassium preparations or salt substitutes containing potassium ions, as well as the use of drugs whose effect is associated with an increase in potassium in blood plasma (e.g., heparin). Periodic monitoring of potassium in the blood plasma is recommended. Angioedema of the face, limbs, lips, tongue, mucous membranes, epiglottis and / or larynx was observed with the use of ACE inhibitors, including preparations containing lisinopril. This side effect can occur at any stage of therapy. In such cases, it is urgent to cancel the use of lisinopril and prescribe adequate therapy. The patient should be under the supervision of a doctor until the regression of symptoms of edema is complete. It should be borne in mind that even in cases where only swelling of the tongue is noted, the patient should be under the supervision of a doctor, since therapy with antihistamines and corticosteroids may be insufficient. Patients who have previously undergone respiratory surgery have a higher risk of developing angioedema of the larynx or tongue. Patients who have undergone angioedema that are not associated with ACE inhibitors are at greater risk of developing such a complication when taking ACE inhibitors. It should be borne in mind that the use of ACE inhibitors in patients of the Negroid race entails a higher risk of developing angioedema. The effectiveness of ACE inhibitors in reducing blood pressure in patients of the Negroid race is lower than in representatives of other races. This effect is probably associated with a pronounced predominance of low-root status in patients of the Negroid race with arterial hypertension. In patients taking ACE inhibitors during the desensitization procedure for hymenoptera venom, life-threatening anaphylactoid reactions can rarely occur. This can be avoided by temporarily discontinuing treatment with an ACE inhibitor before each desensitization procedure. Dry cough that appears when using ACE inhibitors is unproductive, persistent and disappears after treatment is stopped. In the differential diagnosis of cough, its possible relationship with ACE inhibitors should be considered. Very rarely, there have been cases of the development of a syndrome that began with the development of cholestatic jaundice, progressed to fulminant necrosis, and in some cases led to death. The mechanism of development of this syndrome is not clear. The use of lisinopril in patients with signs of jaundice or a significant increase in the activity of hepatic transaminases should be discontinued and appropriate monitoring of laboratory parameters and the patient's condition should be carried out. There have been cases of the development of neutropenia / agranulocytosis, thrombocytopenia and anemia while taking ACE inhibitors. Such cases are quite rare in patients with normal renal function. Neutropenia and agranulocytosis disappear after the withdrawal of ACE inhibitors. Lisinopril should be used with extreme caution in patients with systemic connective tissue diseases receiving immunosuppressive therapy, treatment with allopurinol or procainamide, or these risk factors are present simultaneously, especially in patients with impaired renal function. In such patients, in some cases, infectious diseases that are resistant to antibiotic therapy may develop. If the drug is used in such patients, regular monitoring of blood leukocytes should be carried out. If any symptoms of infection appear (for example, tonsillitis, fever), the patient should immediately consult a doctor, as they can be a manifestation of neutropenia. In rare cases, against the background of therapy with ACE inhibitors, angioedema of the intestine develops. At the same time, patients have abdominal pain as an isolated symptom or in combination with nausea and vomiting, in some cases without previous angioedema of the face and with a normal level of C1 esterase. The diagnosis is made using computed tomography of the abdominal cavity, ultrasound or surgical intervention. Symptoms disappeared after stopping ACE inhibitors. Therefore, in patients with abdominal pain receiving ACE inhibitors, when conducting differential diagnosis, it is necessary to take into account the possibility of developing angioedema of the intestine. Influence on the ability to drive vehicles and control mechanisms During the treatment period, one should refrain from driving vehicles and engaging in potentially dangerous activities that require an increased concentration of attention and speed of psychomotor reactions, since the development of weakness or dizziness is possible, especially at the beginning of the course of treatment.