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Systematic (IUPAC) name
CAS number  ?
ATC code C07AB03
PubChem 2249
DrugBank APRD00172
Chemical data
Formula C14H22N2O3 
Mol. mass 266.336 g/mol
Pharmacokinetic data
Bioavailability 40-50%
Protein binding 6-16%
Metabolism Hepatic <10%
Half life 6-7hours
Excretion Renal
Lactic (In lactiferous females)
Therapeutic considerations
Pregnancy cat.


Legal status

Prescription only

Routes oral iv

Atenolol is a β1 receptor specific antagonist, a drug belonging to the group of 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.

Unlike Propranolol, atenolol does not pass through the blood-brain barrier thus avoiding various CNS side effects.

Whilst atenolol, the most widely used β-blocker in the United Kingdom, was once 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 well than other drugs, particularly in the elderly, and there is increasing evidence that the most frequently used β-blockers at usual doses carry an unacceptable risk of provoking type 2 diabetes.[1]



Atenolol (trade name Tenormin) can be used to treat cardiovascular diseases such as hypertension, coronary heart disease, arrhythmias, and treatment of myocardial infarction after the acute event. Patients with compensated congestive heart failure may be treated with atenolol as a comedication (usually together with an ACE inhibitor, a diuretic and a digitalis-glycoside, if indicated). In patients with congestive heart failure, it reduces the need for and the consumption of oxygen of the heart muscle. It is very important to start with low doses, as atenolol reduces also the muscular power of the heart, which is an undesired effect in congestive heart failure.

The drug is also used to treat the symptoms of other conditions, including dysautonomia, anxiety and hyperthyroidism (overfunction of the thyroid gland).

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).

Atenolol is a so-called β1-selective (or 'cardioselective') drug. That means that it exerts greater blocking activity on myocardial β1-receptors than on β2 ones in the lung. The β2 receptors are responsible to keep 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, particularly with high doses. Extreme caution should be exerted if atenolol is given to asthma patients, who are particularly at risk; the dose should be as low as possible. If an asthma attack occurs, the inhalation of a β2-mimetic antiasthmatic, such as hexoprenalin or salbutamol, will usually suppress the symptoms.

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 particular, diuretics are superior. Propranolol and metoprolol might also be better alternatives. However, controlled studies are lacking.[2]

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. However, preexisting renal insufficience of higher degree makes dose-reductions necessary (see below)


  • bradycardia (pulse less than 50 bpm)
  • cardiogenic shock
  • asthma (may cause broncho-constriction)
  • symptomatic hypotension (blood pressure of less than 100/60 mm Hg with dizziness, vertigo etc.)
  • angina of the Prinzmetal type (vasospastic angina)
  • metabolic acidosis (a severe condition with a more acid 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, very rarely encountered)
  • hypersensitivity and/or allergy to Atenolol
  • Caution: patients with preexisting asthma bronchiale
  • Caution: only if clearly needed during pregnancy, as atenolol may retard fetal growth and possibly causes other abnormalities. (If you are pregnant or plan to become pregnant, ask your doctor.)

Side effects

See also: Propranolol

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.[1]

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.


See also: Propranolol


In patients with normal renal function, the daily dose is 25 to 100 mg (in one dose or in two divided doses) 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.

In patients with chronic heart failure the initial dose should be particularly low and increments should be made slowly.

In patients with a creatinin-clearance (an indicator for renal function) less than (35 ml/min) /1.73 m² the daily dose should be reduced to 25 to 50 mg daily 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 (= low blood sugar) 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.

This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Atenolol". A list of authors is available in Wikipedia.
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