1 : 1 mixture (racemate)
|Systematic (IUPAC) name|
|Licence data||US FDA:|
|Oral or IV|
|Biological half-life||6-7 hours|
Lactic (In lactiferous females)
|ATC code||C07AB03 (WHO)|
|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.
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.
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.
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.
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.
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.
- Agon P, Goethals P, Van Haver D, Kaufman JM (August 1991). "Permeability of the blood–brain barrier for atenolol studied by positron emission tomography". J. Pharm. Pharmacol. 43 (8): 597–600. PMID 1681079. doi:10.1111/j.2042-7158.1991.tb03545.x.
- "Atenolol". The American Society of Health-System Pharmacists. Retrieved 3 April 2011.
- Sheetal Ladva (2006-06-28). "NICE and BHS launch updated hypertension guideline". National Institute for Health and Clinical Excellence.
- Carlberg B, Samuelsson O, Lindholm LH (2004). "Atenolol in hypertension: is it a wise choice?". Lancet. 364 (9446): 1684–9. PMID 15530629. doi:10.1016/S0140-6736(04)17355-8.
- DeLima LG, Kharasch ED, Butler S (1995). "Successful pharmacologic treatment of massive atenolol overdose: sequential hemodynamics and plasma atenolol concentrations". Anesthesiology. 83 (1): 204–207. PMID 7605000. doi:10.1097/00000542-199507000-00025.
- R. Baselt (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, CA: Biomedical Publications. pp. 116–117.
- Hope, Jenny (6 September 2006). "Beta-blockers 'increase diabetes risk by 50 per cent'". London: Daily Mail.