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Systematic (IUPAC) name
Clinical data
  • AU: C
  • US: D (Evidence of risk)
Routes of
Oral or IV
Legal status
Legal status
  • ℞ (Prescription only)
Pharmacokinetic data
Bioavailability 40-50%
Protein binding 6-16%
Metabolism Hepatic <10%
Biological half-life 6-7hours
Excretion Renal
Lactic (In lactiferous females)
CAS Number 29122-68-7
ATC code C07AB03 (WHO)
PubChem CID 2249
DrugBank APRD00172
ChemSpider 2162
Chemical data
Formula C14H22N2O3
Molar mass 266.336 g/mol[[Script error: No such module "String".]]
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Atenolol (Tenormin) 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. The chemical works by slowing down the heart and reducing its workload. Unlike propranolol, atenolol does not pass through the blood-brain barrier thus avoiding 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. Some evidence suggests that even in normal doses the most frequently used β-blockers carry an unacceptable risk of provoking type 2 diabetes.[2]


Atenolol can be used to treat cardiovascular diseases and conditions such as hypertension, coronary heart disease, arrhythmias, angina (chest pain) and to treat and reduce the risk of heart complications following myocardial infarction (heart attack). It is also used to treat the symptoms of Graves Disease, until antithyroid medication can take effect.

Due to its hydrophilic 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 (see below).

Cardioselectivity and asthma

Atenolol is classified as a β1-selective (or 'cardioselective') drug, one that exerts greater blocking activity on myocardial β1-receptors than on β2 receptors in the lung. The β2 receptors are responsible for keeping the bronchial system open. If these receptors are blocked, bronchospasm with serious lack of oxygen in the body can result. However, due to its cardioselective properties, the risk of bronchospastic reactions if using atenolol is reduced compared to nonselective drugs as propranolol. Nonetheless, this reaction may also be encountered with atenolol at high doses. Although traditionally B-blockers have been contraindicated when a person carries a diagnosis of asthma, recent studies have revealed that at moderate doses selective B blockers such as Atenolol are well tolerated.

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.[3]

Unlike most other commonly-used β-blockers, atenolol is excreted almost exclusively by the kidneys. This makes it attractive for use in individuals with end-stage liver disease.

Pharmacokinetic data

  • tcmax = 2 to 4 hours after oral dosing (time elapsed before maximal concentration in the blood plasma is reached)
  • The mean elimination halflife is 6 hours. However, the action of the usual oral dose of 25 to 100 mg lasts over a period of 24 hours.
  • Atenolol is a hydrophilic drug. The concentration found in brain tissue is approximately 15% of the plasma concentration only. The drug crosses the placenta barrier freely. In the milk of breastfeeding mothers, approximately 3 times the plasma concentrations are measured.
  • Atenolol is almost exclusively eliminated renally and is well removable by dialysis. A compromised liver function does not lead to higher peak-activity and/or a longer halflife with possible accumulation.


  • bradycardia (pulse less than 50 bpm)
  • cardiogenic shock
  • asthma (may cause broncho-constriction), although unlikely as atenolol is cardioselective
  • symptomatic hypotension (blood pressure of less than 90/60 mm Hg with dizziness, vertigo etc.)
  • angina of the Prinzmetal type (vasospastic angina)
  • metabolic acidosis (a severe condition with a more acidic blood than normal)
  • severe disorders in peripheral arterial circulation
  • AV-Blockage of second and third degree (a particular form of arrhythmia)
  • acutely decompensated congestive heart failure (symptoms may be fluid retention with peripheral edema and/or abdominal fluid retention (ascites), and/or lung edema)
  • sick sinus syndrome (a particular form of arrhythmia)
  • hypersensitivity and/or allergy to atenolol
  • pheochromocytoma (a rare type of tumor of the adrenal glands)

Caution: patients with preexisting bronchial asthma

Caution: only if clearly needed during pregnancy, as atenolol may retard fetal growth and possibly cause other abnormalities.

Side effects

Atenolol causes significantly fewer central nervous system side effects (depressions, nightmares) and fewer bronchospastic reactions, both due to its particular pharmacologic profile.

It 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.[2]

In addition, β-blockers blunt the usual sympathetic nervous system response to hypoglycemia (i.e. sweating, agitation, tachycardia). These drugs therefore have an ability to mask a dangerously low blood sugar, which further decreases their safety and utility in diabetic patients.

Side effects include:

  • indigestion, constipation
  • dry mouth
  • dizziness or faintness (especially cases of orthostatic hypotension)
  • cold extremities
  • hair loss
  • problems with sexual function
  • runny/blocked nose
  • depression
  • confusion
  • difficulty sleeping, nightmares
  • fatigue, weakness or lack of energy

These side effects may or may not be experienced, but if they are, you should notify your doctor.

More serious side effects can include:

Serious side effects may require urgent medical attention. Some of these side effects are rare and others (not mentioned in the above list) can occur in some people.



In patients with normal renal function, the daily dose is 25 to 50 mg for the management of hypertension depending on the indication and severity of the disease. In most patients, the physician will start with a low initial dose and make increments in weekly intervals as tolerated. Dosage can vary from as little as 25 mg to 200mg a day. In cases of doses over 100mg, the dosage is usually divided and taken twice daily.

For the management of angina, 100mg daily may be given.

In patients with impaired renal function the daily dose should be reduced according to the clinical response of the individual patient. If a patient with end-stage renal failure is scheduled on regular dialysis, usually 50 mg are given after each dialysis procedure. In these patients, a severe hypotension may occur afterwards.

Combination treatment of hypertension

If atenolol alone fails to control arterial hypertension, the drug can be combined with a diuretic (e.g. with chlortalidone in co-tenidone) and/or a vasodilator (hydralazine, or in severe cases minoxidil). Central alpha-agonists (e.g. clonidine), ACE Inhibitors or Angiotensin II receptor antagonists such as losartan can also be given additionally. Exert caution with calcium-antagonists of the verapamil-type as adjunct therapy because of additional negative impact on the muscular strength of the heart. Use of calcium-antagonists of the nifedipine-type is controversial..


Symptoms of overdose are due to excessive pharmacodynamic actions on β1 and also β2-receptors. These include bradycardia, 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.[4][5]

See also


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External links


de:Atenolol es:Atenolol fa:آتنولول fr:Aténolol hr:Atenolol it:Atenololo hu:Atenolol nl:Atenolol pl:Atenolol pt:Atenolol ru:Атенолол uk:Атенолол

Marketed as

  • Myodura-Max(s-amlodipine besylate + Atenolol)in India by Wockhardt Ltd.
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  • 2.0 2.1 Sheetal Ladva (2006-06-30). "Updated NICE guideline on the management of hypertension in adults in primary care". National Institute for Health and Clinical Excellence. Retrieved 2009-02-03. 
  • Carlberg B, Samuelsson O, Lindholm LH (2004). "Atenolol in hypertension: is it a wise choice?". Lancet. 364 (9446): 1684–9. doi:10.1016/S0140-6736(04)17355-8. PMID 15530629. 
  • DeLima LG, Kharasch ED, Butler S. Successful pharmacologic treatment of massive atenolol overdose: sequential hemodynamics and plasma atenolol concentrations. Anesthesiology 83:204-207, 1995.
  • R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 116-117.