|Oral or IV|
|ATC code||C07AB03 (WHO)|
|Biological half-life||6–7 hours|
Lactic (In lactiferous females)
|Chemical and physical data|
|Molar mass||266.336 g/mol|
|3D model (Jmol)||Interactive image|
Atenolol is a selective β1 receptor antagonist, a drug belonging to the group of beta blockers (sometimes written β-blockers), a class of drugs used primarily in cardiovascular diseases. Introduced in 1976, atenolol was developed as a replacement for propranolol in the treatment of hypertension. It works by slowing down the heart and reducing its workload. Unlike propranolol, atenolol does not readily pass through the blood–brain barrier, thus decreasing the incidence of central nervous system side effects.
Atenolol is one of the most widely used β-blockers in the United Kingdom and was once the first-line treatment for hypertension. However, recent studies indicate that atenolol may not reduce morbidity or mortality when used to treat hypertension, and may even increase mortality in some subgroups. In addition, the role for β-blockers in general in hypertension was downgraded in June 2006 in the United Kingdom, and later in the United States, as they are less appropriate than newer drugs, particularly in the elderly.
Atenolol is used for a number of conditions including hypertension, angina, long QT syndrome, acute myocardial infarction, supraventricular tachycardia, ventricular tachycardia, and the symptoms of alcohol withdrawal.
Off-label uses of atenolol, as with other cardioselective β-blockers, include symptomatic treatment of psychological issues such as anxiety. β-blockers are effective for some in treating the somatic (physical) effects of anxiety. In these instances, dosing is used as needed instead of regular daily dosing.
Due to its hydrophilic (water-attracting) properties, the drug is less suitable in migraine prophylaxis compared to propranolol, because, for this indication, atenolol would have to reach the brain in high concentrations, which is not the case, because atenolol does not pass through the blood–brain barrier.
Atenolol was the main β-blocker identified as carrying a higher risk of provoking type 2 diabetes, leading to its downgrading in the United Kingdom in June 2006 to fourth-line agent in the management of hypertension.
Antihypertensive therapy with atenolol provides weaker protective action against cardiovascular complications (e.g. myocardial infarction and stroke) compared to other antihypertensive drugs. In some cases, diuretics are superior. In addition, atenolol has been found to lack mortality benefits and even to increase mortality in older adults.
Symptoms of overdose are due to excessive pharmacodynamic actions on β1 and also β2-receptors. These include bradycardia (slow heartbeat), severe hypotension with shock, acute heart failure, hypoglycemia and bronchospastic reactions. Treatment is largely symptomatic. Hospitalization and intensive monitoring is indicated. Activated charcoal is useful to absorb the drug. Atropine will counteract bradycardia, glucagon helps with hypoglycemia, dobutamine can be given against hypotension and the inhalation of a β2-mimetic as hexoprenalin or salbutamol will terminate bronchospasms. Blood or plasma atenolol concentrations may be measured to confirm a diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Plasma levels are usually less than 3 mg/L during therapeutic administration, but can range from 3–30 mg/L in overdose victims.
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