Systematic (IUPAC) name
Clinical data
Trade names Tenormin
Licence data US FDA:
  • AU: C
  • US: D (Evidence of risk)
Legal status
  • (Prescription only)
Routes of
Oral or IV
Pharmacokinetic data
Bioavailability 40-50%
Protein binding 6-16%
Metabolism Hepatic <10%
Biological half-life 6-7 hours
Excretion Renal
Lactic (In lactiferous females)
CAS Registry Number  YesY
ATC code C07
PubChem CID:
DrugBank  YesY
ChemSpider  YesY
Chemical data
Formula C14H22N2O3
Molecular mass 266.336 g/mol

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 pass through the blood–brain barrier to a large extent thus decreasing the incidence of various central nervous system side effects.[1]

Atenolol is one of the most widely used β-blockers in the United Kingdom and was once the first-line treatment for hypertension. The role for β-blockers in hypertension was downgraded in June 2006 in the United Kingdom to fourth-line, as they perform less appropriately or effectively than newer drugs, particularly in the elderly.


  • Medical uses 1
  • Side effects 2
    • Overdose 2.1
  • References 3
  • External links 4

Medical uses

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.[2]

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.[1]

Side effects

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.[3]

Provisional data suggests that 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. However, controlled studies are lacking.[4]


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. In early cases emesis can be induced. 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.[5][6]


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External links