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Clinical data
Trade namesTenormin, others
License data
  • AU: C
Routes of
oral, Intravenous (IV)
Drug classSelective β1 receptor antagonist
ATC code
Legal status
Legal status
  • AU: S4 (Prescription only)
  • US: WARNING[1]
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Protein binding6–16%[2]
Onset of actionIVTooltip Intravenous injection: <5 minutes[2]
Oral: <1 hour[2]
Elimination half-life6–7 hours[2]
Duration of action>24 hours[2]
ExcretionUrine (>85% IV, 50% oral)[2]
  • (RS)-2-{4-[2-Hydroxy-3-(propan-2-ylamino)propoxy]phenyl}acetamide
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.044.941 Edit this at Wikidata
Chemical and physical data
Molar mass266.341 g·mol−1
3D model (JSmol)
ChiralityRacemic mixture
  • O=C(N)Cc1ccc(cc1)OCC(O)CNC(C)C
  • InChI=1S/C14H22N2O3/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18) checkY

Atenolol is a beta blocker medication primarily used to treat high blood pressure and heart-associated chest pain.[3] Atenolol, however, does not seem to improve mortality in those with high blood pressure.[4][5] Other uses include the prevention of migraines and treatment of certain irregular heart beats.[3][6] It is taken orally (by mouth) or by intravenous injection (injection into a vein).[3][6] It can also be used with other blood pressure medications.[6]

Common side effects include feeling tired, heart failure, dizziness, depression, and shortness of breath.[3] Other serious side effects include bronchial spasm.[3] Use is not recommended during pregnancy[3] and alternative drugs are preferred when breastfeeding.[7] It works by blocking β1-adrenergic receptors in the heart, thus decreasing the heart rate and workload.[3]

Atenolol was patented in 1969 and approved for medical use in 1975.[8] It is on the World Health Organization's List of Essential Medicines.[9] It is available as a generic medication.[3] In 2021, it was the 47th most commonly prescribed medication in the United States, with more than 14 million prescriptions.[10][11]

Medical uses[edit]

Atenolol is used for a number of conditions including hyperthyroidism,[12] hypertension, angina, long QT syndrome, acute myocardial infarction, supraventricular tachycardia, ventricular tachycardia, and the symptoms of alcohol withdrawal.[13]

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 other agents such as ACE inhibitors, calcium channel blockers, thiazide diuretics and angiotensin receptor blockers, particularly in the elderly.[14][15][16]

Side effects[edit]

Hypertension treated with a β-blocker such as atenolol, alone or in conjunction with a thiazide diuretic, is associated with a higher incidence of new onset type 2 diabetes mellitus compared to those treated with an ACE inhibitor or angiotensin receptor blocker. [17][18]

β-blockers, of which atenolol is mainly studied, provides weaker protection against stroke and mortality in patients over 60 years old compared to other antihypertensive medications.[19][20][21][14] Diuretics may be associated with better cardiovascular and cerebrovascular outcomes than β-blockers in the elderly.[22]


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 such 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.[23][24]



Atenolol is a beta blocker, that is, an antagonist of the β-adrenergic receptors.[25][2] It is specifically a selective antagonist of the β1-adrenergic receptor with no intrinsic sympathomimetic activity (i.e., partial agonist activity) or membrane-stabilizing activity.[25][2] However, the preferential action atenolol is not absolute, and at high doses it can also block β2-adrenergic receptors.[2]

Beta-blocking effects of atenolol include reduction in resting and exercise heart rate and cardiac output, reduction of systolic and diastolic blood pressure at rest and with exercise, inhibition tachycardia induced by isoproterenol (a non-selective β-adrenergic receptor agonist), and reduction of reflex orthostatic tachycardia.[2] The beta-blocking effects of atenolol, as measured by reduction of exercise-related tachycardia, are apparent within 1 hour and are maximal within 2 to 4 hours following a single oral dose.[2] The pharmacodynamic effects of atenolol, including beta-blocking and antihypertensive effects, last for at least 24 hours following oral doses of 50 or 100 mg.[2] With intravenous administration, maximal reduction in exercise-related tachycardia occurs within 5 minutes and following a single 10 mg dose has dissipated within 12 hours.[2] The duration of action of atenolol is dose-related and is correlated with circulating levels of atenolol.[2]


The absorption of atenolol with oral administration is rapid and consistent but is incomplete.[2] About 50% of an oral dose of atenolol is absorbed from the intestines, with the rest excreted in feces.[2] Maximal concentrations of atenolol occur 2 to 4 hours following an oral dose, whereas peak concentrations occur within 5 minutes with intravenous administration.[2] The pharmacokinetic profile of atenolol results in it having relatively consistent plasma drug levels with about 4-fold variation between individuals.[2]

The plasma protein binding of atenolol is 6 to 16%.[2] Atenolol is classified as a beta blocker with low lipophilicity and hence lower potential for crossing the blood–brain barrier and entering the brain.[25] This in turn may result in fewer effects in the central nervous system as well as a lower risk of neuropsychiatric side effects.[25]

Atenolol undergoes little to no metabolism by the liver.[2] This is in contrast to other beta blockers like propranolol and metoprolol, but is similar to nadolol.[2] Instead of hepatic metabolism, atenolol is eliminated mainly via renal excretion.[2] Atenolol is excreted 50% in urine with oral administration and more than 85% in urine with intravenous administration.[2]

The elimination half-life of atenolol is about 6 to 7 hours.[2] The half-life of atenolol does not change with continuous administration.[2] With intravenous administration, atenolol levels rapidly decline (5- to 10-fold) during the first 7 hours and thereafter decline at a rate similar to that with oral administration.[2] The elimination of atenolol is slowed in renal impairment, with the elimination rate being closely related to the glomerular filtration rate and with significant accumulation occurring when the creatinine clearance rate is under 35 mL/min/1.73 m2.[2]

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 not as effective as others in treating some conditions.[26] In 2012, 33.8 million prescriptions were written to American patients for this drug.[26] In 2014, it was in the top (most common) 1% of drugs prescribed to Medicare patients.[26] Although the number of prescriptions has been declining steadily since limited evidence articles contesting its efficacy was published, it has been estimated that it would take 20 years for doctors to stop prescribing it for hypertension.[26] Despite its diminished efficacy when compared to newer antihypertensive drugs, atenolol and other beta blockers are still a relevant clinical choice for treating some conditions, since beta blockers are a diverse group of medicines with different properties that still requires further research.[14] As consequence, reasons for the popularity of beta blockers cannot be fully attributed to a slow healthcare system – patient compliance factor, such as treatment cost and duration, also affect adherence and popularity of therapy.[27]


  1. ^ "FDA-sourced list of all drugs with black box warnings (Use Download Full Results and View Query links.)". FDA. Retrieved 22 October 2023.
  2. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab "DailyMed - TENORMIN- atenolol tablet". DailyMed. 30 June 2021. Archived from the original on 27 January 2022. Retrieved 20 November 2023.
  3. ^ a b c d e f g h "Atenolol Monograph for Professionals". AHFS. Archived from the original on 18 April 2019. Retrieved 23 December 2018.
  4. ^ 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 3941231. PMID 24672712.
  5. ^ DiNicolantonio JJ, Fares H, Niazi AK, Chatterjee S, D'Ascenzo F, Cerrato E, et al. (2015). "β-Blockers in hypertension, diabetes, heart failure and acute myocardial infarction: a review of the literature". Open Heart. 2 (1): e000230. doi:10.1136/openhrt-2014-000230. PMC 4371808. PMID 25821584.
  6. ^ a b c British national formulary : BNF 76 (76 ed.). Pharmaceutical Press. 2018. pp. 151–153. ISBN 9780857113382.
  7. ^ "Atenolol use while Breastfeeding". Archived from the original on 23 December 2018. Retrieved 23 December 2018.
  8. ^ Fischer J, Ganellin CR (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 461. ISBN 9783527607495.
  9. ^ World Health Organization (2021). World Health Organization model list of essential medicines: 22nd list (2021). Geneva: World Health Organization. hdl:10665/345533. WHO/MHP/HPS/EML/2021.02.
  10. ^ "The Top 300 of 2021". ClinCalc. Archived from the original on 15 January 2024. Retrieved 14 January 2024.
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  12. ^ Rehman B, Sanchez DP, Shah S (2021). "Atenolol". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 30969666. Archived from the original on 10 October 2022. Retrieved 5 September 2021.
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  14. ^ a b c Wiysonge CS, Bradley HA, Volmink J, Mayosi BM, Opie LH (January 2017). "Beta-blockers for hypertension". The Cochrane Database of Systematic Reviews. 1 (1): CD002003. doi:10.1002/14651858.CD002003.pub5. PMC 5369873. PMID 28107561. Further research should be of high quality and should explore whether there are differences between different subtypes of beta-blockers or whether beta-blockers have differential effects on younger and older people [...] Beta-blockers were not as good at preventing the number of deaths, strokes, and heart attacks as other classes of medicines such as diuretics, calcium-channel blockers, and renin-angiotensin system inhibitors. Most of these findings come from one type of beta-blocker called atenolol. However, beta-blockers are a diverse group of medicines with different properties, and we need more well-conducted research in this area." (p. 2-3)
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  17. ^ Lindholm LH, Ibsen H, Borch-Johnsen K, Olsen MH, Wachtell K, Dahlöf B, et al. (September 2002). "Risk of new-onset diabetes in the Losartan Intervention For Endpoint reduction in hypertension study". Journal of Hypertension. 20 (9): 1879–86. doi:10.1097/00004872-200209000-00035. PMID 12195132. S2CID 23613019.
  18. ^ Elliott WJ, Meyer PM (January 2007). "Incident diabetes in clinical trials of antihypertensive drugs: a network meta-analysis". Lancet. 369 (9557): 201–7. doi:10.1016/s0140-6736(07)60108-1. PMID 17240286. S2CID 37044384.
  19. ^ Lindholm LH, Carlberg B, Samuelsson O (October 2005). "Should β blockers remain first choice in the treatment of primary hypertension? A meta-analysis". The Lancet. 366 (9496): 1545–1553. doi:10.1016/S0140-6736(05)67573-3. PMID 16257341. S2CID 34364430.
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  21. ^ Kuyper LM, Khan NA (May 2014). "Atenolol vs nonatenolol β-blockers for the treatment of hypertension: a meta-analysis". The Canadian Journal of Cardiology. 30 (5 Suppl): S47-53. doi:10.1016/j.cjca.2014.01.006. PMID 24750981.
  22. ^ Messerli FH, Grossman E, Goldbourt U (June 1998). "Are beta-blockers efficacious as first-line therapy for hypertension in the elderly? A systematic review". JAMA. 279 (23): 1903–7. doi:10.1001/jama.279.23.1903. PMID 9634263.
  23. ^ DeLima LG, Kharasch ED, Butler S (July 1995). "Successful pharmacologic treatment of massive atenolol overdose: sequential hemodynamics and plasma atenolol concentrations". Anesthesiology. 83 (1): 204–7. doi:10.1097/00000542-199507000-00025. PMID 7605000.
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  27. ^ Choi HY, Oh IJ, Lee JA, Lim J, Kim YS, Jeon TH, et al. (November 2018). "Factors Affecting Adherence to Antihypertensive Medication". Korean Journal of Family Medicine. 39 (6): 325–332. doi:10.4082/kjfm.17.0041. PMC 6250947. PMID 30384549.