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									  At Beta

                                         At Beta

                              Systematic (IUPAC) name


                                      Chemical data

   Formula            C14H22N2O3

                                   Pharmacokinetic data

Bioavailability       40-50%

Protein binding       6-16%

 Metabolism           Hepatic <10%

   Half-life          6-7hours

  Excretion           Renal
                      Lactic (In lactiferous females)

 Legal status         ℞ Prescription only

    Routes            Oral or IV
At Beta 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, At Beta 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, At Beta does not pass through
the blood-brain barrier thus avoiding 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. Some evidence
suggests that even in normal doses the most frequently used β-blockers carry an
unacceptable risk of provoking type 2 diabetes.



At Beta 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, At Beta would have to reach the
brain in high concentrations, which is not the case (see below).

Cardioselectivity and asthma

At Beta 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 At Beta
is reduced compared to nonselective drugs as propranolol. Nonetheless, this reaction
may also be encountered with At Beta 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 At Beta are well

Provisional data suggests that antihypertensive therapy with At Beta 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.
Unlike most other commonly-used β-blockers, At Beta is excreted almost exclusively by
the kidneys. This makes it attractive for use in individuals with end-stage liver disease.

Combination treatment of hypertension

If At Beta 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..

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.
      At Beta 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.
      At Beta 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 At Beta is
      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 At Beta
      pheochromocytoma (a rare type of tumor of the adrenal glands)
Caution: patients with preexisting bronchial asthma

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

Side effects

See also: Beta blocker

At Beta 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

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:

      hallucinations
      low blood pressure (hypotension)
      skin reactions, e.g. rash, hives, flaking of skin, worsening of psoriasis
      sensation of 'pins and needles' hands or feet
      irritated eyes, visual disturbances
      difficulty hearing
      difficulty speaking
      unsteadiness when walking

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 200 mg a day. In
cases of doses over 100 mg, the dosage is usually divided and taken twice daily.

For the management of angina, 100 mg 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.


Symptoms of overdose are due to excessive pharmacodynamic actions on β 1 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 At Beta 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.

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