Synonym(s)
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 with an accumulation of bradykinin and substance P, among other things; no tolerance phenomena are to be expected here, these side effects often lead to discontinuation of therapy). Cough can 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)
Furthermore:
- 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 disorders (1-3%), upper abdominal complaints (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 (often accompanied by physical urticaria), which may manifest late and is extremely resistant to therapy.
- Less common is the occurrence of exsiccation eczema (especially in combination with advanced age)
- Angioedema: Angioedema (AE/0.01-0.1%) acquired through the use of ACE inhibitors is important from a dermatological/allergological point of view. This side effect occurs mainly in patients with a deficiency of aminopeptidase P (this enzyme is responsible for the degradation of bradykinin together with ACE). AE symptoms mainly occur after the first month of ACE treatment. However, very late cases are also described in the literature, sometimes after several years of stable therapy. It has been observed that patients previously stably treated with ACE inhibitors developed AE after the addition of another drug, including the combination of aspirin or non-steroidal anti-inflammatory drugs with ACE inhibitors. Attention should be drawn to this sometimes very late and rare side effect of ACE inhibitors. ACE-induced angioedema is best treated with 30mg Icatibant (antagonist of the bradykinin B2 receptor).
- Further side effects can be found 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