What Are the Most Common Side Effects of ACE Inhibitors?

Angiotensin-converting enzyme inhibitor (ACEI) is a compound that inhibits angiotensin-converting enzyme activity. Angiotensin-converting enzyme catalyzes angiotensin I to produce angiotensin II, which is a potent vasoconstrictor and activator of adrenal aldosterone release.

Drug Name: Angiotensin converting enzyme inhibitor
Alias: ACEI

Foreign name: ACE inhibitor
Main indications: Hypertension, heart failure, glomerular disease
Adverse reactions: Cough, abnormal taste, granulocytopenia, rash, fever

Overview of angiotensin-converting enzyme inhibitors

angiotensin converting enzyme inhibitors; ACE inhibitors; ACEI

A compound that inhibits angiotensin-converting enzyme (EC3.4.15.1) activity.

ACEI controls hypertension by inhibiting angiotensin II biosynthesis.

Clinical application of angiotensin converting enzyme inhibitor

Angiotensin-converting enzyme inhibitors for hypertension

Renal ischemia stimulates the peripheric cells on the glomerular afferent arteries to secrete renin, which acts on angiotensinogen synthesized by the liver to form angiotensin , which forms blood vessels under the action of angiotensin-converting enzymes. Angiotensin , angiotensin has a strong vasoconstrictive effect, and its vasoconstrictive effect is 10 to 20 times that of epinephrine. Angiotensin can also make the adrenal cortex globular zone secrete aldosterone, promote water and sodium retention, and eventually produce hypertension. The renin-angiotensin-aldosterone system has multiple effects on the occurrence and development of hypertension. After ACEI administration, the peripheral blood vessels dilate, the total peripheral resistance is reduced, and the blood pressure is reduced. At the same time, the blood pressure of the heart, brain, kidney and other important organs is not reduced, the sympathetic nerve reflex function is not disturbed, orthostatic hypotension is not caused. The antihypertensive effect of renin and normal renin hypertension is significant, and it also has antihypertensive effect on low renin hypertension. Long-term application can retreat left ventricular hypertrophy, which usually takes effect within 15 minutes and peaks in 1 to 2 hours.

Angiotensin-converting enzyme inhibitors for heart failure

There are many reasons for heart failure. The activation of the renin-angiotensin-aldosterone system causes contraction of blood vessels and the enhancement of positive myocardial muscle strength. It promotes the release of norepinephrine from sympathetic nerve endings and increases the secretion of aldosterone and vasopressin. Promote the adrenal gland to produce deoxycorticosterone, promote the release and degradation of kallikrein, and make potassium sodium excretion, water and sodium retention. These results make myocardial hypertrophy accompanied by apoptosis of myocardial cells, vasoconstriction, and increase in circulating blood volume. Aggravating, ACEI reduces the anterior and posterior load of the heart by reducing the effects of angiotensin and aldosterone, reduces the resistance of peripheral blood vessels and coronary vessels, increases coronary blood supply, reduces myocardial fibrosis, and slows myocardial cell apoptosis. It is used to treat refractory heart failure and asymptomatic heart failure, and it also has good curative effect on heart failure patients who are ineffective with digitalis, diuretics and vasodilators.

Angiotensin-converting enzyme inhibitors for glomerular disease

An independent factor that affects the prognosis of glomerular disease is proteinuria. In addition to long-term large amounts of proteinuria causing hypoproteinemia, it can also cause glomerular and tubular toxicity and inflammatory reactions. Long-term hypertension and increased glomerular pressure can damage renal function, which is an important factor affecting the prognosis of various glomerular diseases. Lowering systemic blood pressure and glomerular pressure can effectively alleviate the progress of renal disease. ACEI can reduce the systemic blood pressure and intrarenal blood pressure, improve the permeability of the glomerular filtration membrane, reduce the excretion of proteinuria, and inhibit the hardening process of renal tissue cells, including mesangial cells, endothelial cells and tubular epithelial cells, and interstitial cells. Plasma fibroblasts proliferate and secrete chemokines, inflammatory factors, and fibroblasts, thereby inhibiting the inflammatory response and sclerosis of renal tissues. Most patients have reduced proteinuria after 4 to 5 days of medication, and long-term medication can reduce proteinuria by 45%.

Angiotensin converting enzyme inhibitor side effects

The adverse reactions of this class of drugs are mild, especially the second generation without thiol groups such as ilapril, lisinopril, cilapril, etc.

Side effects related to angiotensin and obstruction of aldosterone production include hypotension, transient proteinuria, hyperkalemia, sinus bradycardia, headache, etc. These side effects quickly disappear with the prolongation of medication, and generally do not need to be treated.

Side effects related to bradykinin and prostaglandin activation include angioedema, pharyngeal discomfort, irritated dry cough, hoarseness, hiccup, etc. Angioedema should be discontinued in time, and irritated dry cough is common, with prolonged medication time Can alleviate disappearance.

side effects related to the structure of the drug. Captopril contains sulfhydryl groups which can cause granulocytopenia, decreased taste or loss, allergic dermatitis, transient proteinuria, itchy skin, and fever. Second-generation ACEI, such as ilapril, does not contain sulfhydryl groups without this side effect.

Others. Hair loss, gynecomastia, teratology, etc.

Angiotensin-converting enzyme inhibitor drug interactions

Excessive hypotension may occur when ACEI is used in combination with diuretics, other antihypertensives, or agents including blood pressure-lowering ethanol. ACEI may increase blood potassium when combined with potassium-sparing drugs, potassium supplements (including potassium-containing salt substitutes), or other drugs that cause hyperkalemia (such as cyclosporine or indomethacin). For additional effects, serum potassium concentrations should be monitored. Patients with heart failure should generally stop using potassium-sparing diuretics and potassium supplements before using ACEI. However, patients with potassium-releasing diuretics may need potassium supplements for ACEI treatment and serum potassium concentrations should be monitored. The adverse effects of ACEI on the kidney may be enhanced by other drugs, such as NSAIDs, which can affect renal function.

Angiotensin converting enzyme inhibitor pharmacokinetics

Most ACEIs are administered orally. Except for captopril and lisinopril, they are generally prodrugs. After absorption, the esters are hydrolyzed by rapid metabolism and become active diacid forms. Metabolism occurs mainly in the liver. Active drugs or active metabolites are mainly excreted through the urine; Benazepril and Fosinopril can also be excreted through the biliary tract. Elimination of the diacid is heterogeneous, and there is an extended final elimination phase, which is believed to indicate that the drug binds to a saturated binding site on angiotensin. This combination does not lead to drug accumulation after taking double doses. The final elimination half-life cannot predict the kinetics measured after taking the double dose, and the half-life effective for accumulation is often cited as valuable data.

Angiotensin converting enzyme inhibitors clinical principles

ACEI is an antihypertensive drug that acts as a vasodilator and reduces peripheral resistance. It inhibits angiotensin-converting enzyme (ACE), which acts during the conversion of angiotensin I to angiotensin II. Angiotensin II stimulates the synthesis and secretion of aldosterone and raises hypertension through a powerful direct vasoconstriction effect. ACE is the same substance as bradykinin (kininase II). ACEI can also reduce the degradation of bradykinin. (Bradykinin directly relaxes blood vessels and is involved in the production of prostaglandins.) It is believed that the pharmacological effects of ACEI depend on the inhibition of the renin-angiotensin-aldosterone system (RAAS), but it can also be used in patients with low renin Effectively lowers blood pressure, so there are likely to be other mechanisms at work. ACEI reduces both preload and postload in patients with heart failure. It also reduces left ventricular remodeling (sometimes after myocardial infarction). ACEI drugs can reduce the glomerular filtration rate to varying degrees, resulting in increased levels of serum creatinine, which is more likely to occur in patients with basic renal insufficiency and heart failure. ACEI also reduces proteinuria associated with glomerulonephropathy.

ACEI can be used to treat hypertension and heart failure, improve survival after myocardial infarction, and prevent cardiovascular events in patients with identified risk factors. It can also be used for the treatment of diabetic nephropathy. Usually oral administration. Some hypertensive patients may experience a sudden drop in blood pressure after starting the drug, so the first dose is best before bedtime; if possible, stop diuretic treatment a few days before using ACEI, and then recover if necessary. Severe hypotension is common in patients with heart failure who take myelin diuretics for the first time, but temporarily discontinuing diuretics can cause rebound pulmonary edema. Therefore, treatment should be started at low doses and closely monitored.