DefinitionThis section has been translated automatically.
Short name for competitive inhibitors of the angiotensin-converting enzyme (ACE). ACE inhibitors are drugs that are used primarily in the therapy of arterial hypertension and chronic heart failure.
When the blood pressure drops, the so-called "RAAS"(renin-angiotensin-aldosterone system) is activated. This is a cascade-like, interacting enzyme-hormone system that regulates blood pressure in a highly differentiated manner via various mechanisms (increase in blood volume, vasoconstrictive effect). The system is activated by the release of renin in the kidneys, a protein-splitting enzyme that triggers a whole series of reactions. One of the reactions is the conversion of angiotensin I into the peptide angiotensin II. This reaction is catalysed by the angiotensin converting enzyme (ACE).
ACE inhibitors block ACE, which means that angiotensin II, which is important for the regulation of blood pressure, is not produced or is produced in a reduced form. ACE inhibitors block this enzyme, which means that angiotensin II, which is important for the regulation of blood pressure, is not produced or is produced in a reduced form.
Nephroprotective effect ACE inhibitors: they lower the tone of the afferent arterioles in the glomerulum more than in afferent arterioles. This results in a reduction of the gelomerular filtration pressure.
The main agents used in therapy are captopril, enalapril, lisinopril and ramipril.
Pharmacodynamics (Effect)This section has been translated automatically.
Inhibition of angiotensin converting enzyme(ACE) leads to decreased angiotensin II production from angiotensin I. In addition, the degradation of bradykinin is inhibited and leads to its accumulation (see side effects).
In renal diseases such as diabetic nephropathy, ACE inhibitors lead to decreased protein excretion (proteinuria) and prevent progression of the disease (nephroprotection).
Myocardial infarction: Patients with myocardial infarction always benefit from therapy with ACE inhibitors. Treatment should begin between days 2 and 7 after the infarction event and should be continued for an indefinite period whenever left ventricular dysfunction is demonstrable.
A severe drop in blood pressure (in 1% of patients) may occur at the start of therapy. This occurs when there is high activity of the renin-aldosterone system (Cave: Pat. must be monitored initially for several hours). This phenomenon of the first dose can be prevented with a gradual therapy.
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IndicationThis section has been translated automatically.
As monotherapeutics or in combination with diuretics or calcium antagonists for the treatment of hypertensive heart disease. Also used in chronic heart failure and diabetic nephropathy.
Undesirable effectsThis section has been translated automatically.
Dry cough, asthmoid complaints (the side effects are associated, among others, with an accumulation of bradykinin and substance P; no tolerance phenomena are to be expected here, these side effects not infrequently lead to discontinuation of therapy). Cough may be suppressed by sodium cromoglicate.
Hepatotoxic side effects (1%); increase in liver-specific enzymes; signs of cholestasis Throm
Reversible increase in serum creatinine
Blood count changes (leukopenia, neutropenia, thrombocytopenia).
- Hypotension, acute renal failure, hyperkalemia, urticarial exanthema (0.1-1% of cases) and urticaria (0.01-0.1%).
- Central nervous complaints such as headache, drowsiness, and dizziness.
- gastrointestinal disturbances (1-3%), upper abdominal discomfort (reports of isolated visceral angioedema are available)
- Hyperkalemia (clinically relevant hyperkalemia occurs in < 10% of cases. Cave: potassium-retarding diuretics!).
- Pruritus: It is not uncommon for ACE inhibitors to cause pruritus, which may manifest late and is extremely resistant to therapy (often accompanied by physical urticaria).
- Angioedema: From a dermatological/allergological point of view, the angioedema (AE/0.01-0.1%) acquired by the use of ACE inhibitors is important. This side effect occurs mainly in patients deficient in aminopeptidase P (this enzyme, together with ACE, is responsible for the degradation of bradykinin). AE symptoms occur mainly after the first month of ACE treatment. However, very late-onset cases have also been described in the literature, sometimes after several years of stable therapy. It has been observed that patients previously treated stably with ACE inhibitors developed AE after the addition of another drug, including the combination of aspirin or nonsteroidal anti-inflammatory drugs with ACE inhibitors. This sometimes very late and rare side effect of ACE inhibitors should be noted. ACE-induced angioedema is best treated with 30mg Icatibant (antagonist of the bradykinin B2 receptor).
- For further side effects, see under the individual preparations.
InteractionsThis section has been translated automatically.
ACE inhibitors intensify the haematological side effects of immunosuppressive drugs (immunosuppressants, cytostatics and glucocorticoids)
ContraindicationThis section has been translated automatically.
PreparationsThis section has been translated automatically.
Examples of active ingredients and preparations from the group of ACE inhibitors:
- Benazepril (Cibacen, generic products)
- Captopril (Lopirin, Tensobon, generic drugs)
- Cilazapril (dynorm)
- Enalapril (Xanef, Pres, generic drugs)
- Fosinopril (Fosinorm, Dynacil)
- Imidapril (Tanatril)
- Lisinopril (Acerbon, Coric, generic products)
- Moexipril (Fempress)
- Perindopril (Coversum, Preterax)
- Quinapril (Accupro, generic products)
- Ramipril (Delix, Vesdil, generic products)
- Spirapril (Quadropril)
- Trandolapril (Gopten, Udrik).
Note(s)This section has been translated automatically.
In Germany, about 20% of the population and every second person over 55 years of age takes drugs to treat high blood pressure. About 35% of hypertension patients are treated with an ACE inhibitor in monotherapy and about 55% in combination with another blood pressure lowering drug.
In the case of angioedema triggered by ACEI, switching to an AT1 receptor blocker is not a solution to the problem, as these can also trigger angioedema (although less frequently than ACEI).
LiteratureThis section has been translated automatically.
- Graefe KH et al. Pharmak with effects on the vascular system. In: Graefe KH et al. (Eds) Pharmacology and Toxicology. Georg Thieme Publisher Stuttgart S.172-173
- Wedi B et al.(2011) Pharmacoprophylaxis and concomitant medication for specific immunotherapy. Dermatologist 62: 663-670