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Atenolol 3d structure.png
Clinical data
Trade names Tenormin
AHFS/ Monograph
MedlinePlus a684031
License data
  • AU: C
  • US: D (Evidence of risk)
Routes of
Oral or IV
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
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 Number
PubChem CID
ECHA InfoCard 100.044.941
Chemical and physical data
Formula C14H22N2O3
Molar mass 266.336 g/mol
3D model (JSmol)
Chirality Racemic mixture

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.[1]

Atenolol is one of the most widely used β-blockers in the United Kingdom and was once the first-line treatment for hypertension.[citation needed] Atenolol is effective at reducing blood pressure, but recent studies indicate that it does not reduce the morbidity or mortality caused by hypertension, and may even increase mortality in some subgroups.[2] This means that when people take this drug, they get better blood pressure numbers, but they still die of heart attacks and strokes, despite the lower blood pressure.

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 blood pressure medications including calcium channel blockers, thiazide diuretics, angiotension converting enzyme (ACE) inhibitors, and angiotension receptor blockers, particularly in the elderly.[citation needed]

Medical uses[edit]

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.[3]

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.[1]

Side effects[edit]

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.[4]

Antihypertensive therapy with atenolol provides weaker protective action against cardiovascular complications (e.g. myocardial infraction and stroke) compared to other antihypertensive drugs. In some cases, diuretics are superior.[5] In addition, atenolol has been found to lack mortality benefits[6][7] and even to increase mortality in older adults.[2]


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.[8][9]

Society and culture[edit]

Atenolol has been given as an example of how slow healthcare providers are to change their prescribing practices in the face of medical evidence that indicates that a drug is ineffective.[10] In 2012, 33.8 million prescriptions were written to American patients for this drug.[10] In 2014, it was in the top (most common) 1% of drugs prescribed to Medicare patients.[10] Although the number of prescriptions has been declining steadily since the evidence against its efficacy was published, it has been estimated that it would take 20 years for doctors to stop prescribing it for hypertension.[10]


  1. ^ a b Agon P, Goethals P, Van Haver D, Kaufman JM (August 1991). "Permeability of the blood–brain barrier for atenolol studied by positron emission tomography". Journal of Pharmacy and Pharmacology. 43 (8): 597–600. doi:10.1111/j.2042-7158.1991.tb03545.x. PMID 1681079. 
  2. ^ a b Testa G, Cacciatore F, Della-Morte D, Mazzella F, Mastrobuoni C, Galizia G, Gargiulo G, Rengo F, Bonaduce D, Abete P (2014). "Atenolol use is associated with long-term mortality in community-dwelling older adults with hypertension". Geriatrics & Gerontology International. 14: 153–8. doi:10.1111/ggi.12073. PMID 23581644. 
  3. ^ "Atenolol". The American Society of Health-System Pharmacists. Retrieved 3 April 2011. 
  4. ^ Sheetal Ladva (28 June 2006). "NICE and BHS launch updated hypertension guideline". National Institute for Health and Clinical Excellence. Archived from the original on 17 June 2008. 
  5. ^ Carlberg B, Samuelsson O, Lindholm LH (2004). "Atenolol in hypertension: is it a wise choice?". The Lancet. 364 (9446): 1684–9. doi:10.1016/S0140-6736(04)17355-8. PMID 15530629. 
  6. ^ Tomiyama H, Yamashina A (2014). "Beta-Blockers in the Management of Hypertension and/or Chronic Kidney Disease". International Journal of Hypertension. 2014: 919256. doi:10.1155/2014/919256. PMC 3941231Freely accessible. PMID 24672712. 
  7. ^ DiNicolantonio JJ, Fares H, Niazi AK, Chatterjee S, D'Ascenzo F, Cerrato E, Biondi-Zoccai G, Lavie CJ, Bell DS, O'Keefe JH (2015). "β-Blockers in hypertension, diabetes, heart failure and acute myocardial infarction: a review of the literature". Open Heart. 2: e000230. doi:10.1136/openhrt-2014-000230. PMC 4371808Freely accessible. PMID 25821584. 
  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. doi:10.1097/00000542-199507000-00025. PMID 7605000. 
  9. ^ R. Baselt (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, Calif.: Biomedical Publications. pp. 116–117. 
  10. ^ a b c d Epstein, David (2017-02-22). "When Evidence Says No, But Doctors Say Yes". ProPublica. Retrieved 2017-02-24.