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A Review On Atenolol: Volume 9, Issue 3, 902-914 Review Article ISSN 2278 - 4357
A Review On Atenolol: Volume 9, Issue 3, 902-914 Review Article ISSN 2278 - 4357
A REVIEW ON ATENOLOL
Ajesh Chauhan*
Beta blockers don’t permanently change blood pressure and chest pain. Instead, they help to
manage the symptoms.
Atenolol belongs to beta blocker class of drugs. A class of drugs is a group of medications
that work in a similar way. These drugs are often used to treat similar conditions. Atenolol is
a cardioselective β-blocker, selective β1 adrenergic antagonist. Atenolol was first introduced
in 1976 and has been approved by the US FDA from August 1981 as a therapeutic agent for
both hypertension and coronary artery disease. Atenolol is one of the most commonly
prescribed betablockers all over the world with more than 40 million prescriptions per year in
the US alone.
It is widely used in the treatment of hypertension and angina pectoris, arrhythmias and
myocardial infarction. This is also used for prophylactic treatment of migraine. It was
specifically developed to pass through the blood brain barrier. Atenolol being a cardio
selective beta blocker does not show adverse effects when given to patients suffering from
bronchial asthma and diabetes mellitus. Patient compliance is better with atenolol because it
is given once a day. It is also used to treat other conditions including dysautonomia, anxiety
and hyperthyroidism.[1-6]
is a relatively polar hydrophilic compound with water solubility of 26.5 mg/ml at 370c and a
log partition coefficient (octanol / water) of 0.23. Atenolol is a white or almost white powder.
It is sparingly soluble in water; soluble in ethanol (~750 g/L) TS; slightly soluble in
dichloromethane R.[7, 8]
Pharmacokinetics
Atenolol is a β1 selective antagonist with lowest lipid solubility among all betablockers. It
differs from Pindolol and Proponolol in that it does not have an intrinsic sympathomimetic
action or membrane stabilising activity. It acts by competing with catecholamines for binding
at β1 adrenergic receptors in the heart and vascular smooth muscle, thus inhibiting
sympathetic stimulation. This results in reduction in heart rate, cardiac output, systolic and
diastolic blood pressure. Reduction in peripheral resistance is gradually seen with chronic
therapy. Endocrine and metabolic actions of Atenolol include lowering of plasma renin
activity and free fatty acid levels. Although Atenolol may prolong insulin-induced
hypoglycemia, this is less than that of nonselective beta-blockers. Atenolol has a complex
effect on lipid metabolism; however, it’s less than that of other nonselective betablockers.
betablockers have a little effect on LdL but do increase plasma VLdL and triglyceride levels
and 4 lower plasma HdL levels. Atenolol is hydrophilic, hence, relatively lower
concentrations are found in brain tissue. Absorption after an oral dose is often incomplete and
peak plasma levels are obtained 2 – 4 hours later. Although plasma, half- life is 6 – 8 hours, it
is increased in renal failure as the major route of excretion is through the kidneys.[9]
Pharmacodynamics[12]
Atenolol is a β-adrenoceptor blocking drug without partial agonist (sympathomimetic) or
membrane stabilising properties. It appears to be relatively selective for cardiac β1-receptors,
although some deterioration in airway function can occur in patients with asthma receiving
atenolol, as with other cardioselective β-blockers. However, such changes are clearly less
severe than those seen with non-selective β-blockers, such as propranolol, and in some
studies atenolol had a lesser effect than the other cardioselective β-blockers. Atenolol can be
cautiously administered to patients with obstructive airways disease provided the patient also
receives treatment with optimal doses of a β2-adrenoceptor agonist bronchodilator drug.
When administered to hypertensive patients (usually with mild to moderate essential
hypertension) in studies which were essentially pharmacodynamic investigations, atenolol
reduced both systolic and diastolic blood pressures by about 15%. The dose-response curve in
such studies was relatively flat, suggesting that the use of a fixed dose may be justifiable in
most patients. The maximum effect usually occurred with a dose of 100 or 200mg, most of
the antihypertensive effect occurring by the third day of treatment. As with other β-blockers,
the reduction in blood pressure with atenolol is consistently accompanied by a reduction in
heart rate (about 15 to 25%) and cardiac output (usually about 20%). Atenolol is a β-
adrenoceptor blocking drug without partial agonist (sympathomimetic) or membrane
stabilising properties. It appears to be relatively selective for cardiac β1-receptors, although
some deterioration in airway function can occur in patients with asthma receiving atenolol, as
with other cardioselective β-blockers. However, such changes are clearly less severe than
those seen with non-selective β-blockers, such as propranolol, and in some studies atenolol
had a lesser effect than the other cardioselective β-blockers. Atenolol can be cautiously
administered to patients with obstructive airways disease provided the patient also receives
treatment with optimal doses of a β2-adrenoceptor agonist bronchodilator drug. When
administered to hypertensive patients (usually with mild to moderate essential hypertension)
in studies which were essentially pharmacodynamic investigations, atenolol reduced both
systolic and diastolic blood pressures by about 15%. The dose-response curve in such studies
was relatively flat, suggesting that the use of a fixed dose may be justifiable in most patients.
The maximum effect usually occurred with a dose of 100 or 200mg, most of the
antihypertensive effect occurring by the third day of treatment. As with other β-blockers, the
reduction in blood pressure with atenolol is consistently accompanied by a reduction in heart
rate (about 15 to 25%) and cardiac output (usually about 20%). In patients with coronary
artery disease, atenolol produces changes in myocardial blood flow which resemble those
seen with other β-blockers, regional myocardial blood flow beingdecreased in both normal
and poststenotic areas but to a slightly greater extent in poststenotic areas. Resting
myocardial oxygen consumption is also reduced in such patients, as is seen with other β-
blockers. As is expected with a β-blocking drug lacking partial agonist activity, atenolol
increases AV conduction time (by about 15%). Sinus cycle length, sinus node recovery time
and atrial refractoriness are also similarly increased.
Uses[11]
Labeled indications
Acute MI: Management of hemodynamically stable patients with definite or suspected acute
MI to reduce cardiovascular mortality.
Thyrotoxicosis
Beta-blockers, including atenolol, are effective and recommended in the treatment of
symptomatic thyrotoxicosis. Beta-blockers should also be considered in asymptomatic
patients who are at increased risk of complications due to worsening hyperthyroidism.
Ventricular arrhythmias
In patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), data from
observational studies suggest that atenolol may be beneficial at reducing ventricular
arrhythmias [Marcus 2009]. The American Heart Association/American College of
Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guideline for management of patients
with ventricular arrhythmias and prevention of sudden cardiac death recommends beta-
blocker therapy in patients with ARVC and history of ventricular arrhythmia and suggests
that beta-blockers may be considered in patients without a history of ventricular arrhythmia.
In patients with congenital long QT syndrome, data from observational studies suggest that
beta-blockers may be beneficial at reducing the risk of cardiac events, including ventricular
Based on the beta-blockers are effective for control of ventricular arrhythmias and ventricular
premature beats.
Dosage[10]
Hypertension
Adult: 25-50 mg/day orally initially; may be increased to 100 mg/day orally
Pediatric (Off-label): 0.5-1 mg/kg/day orally; not to exceed 2 mg/kg/day or 100 mg/day
Geriatric: 25 mg/day orally initially; may be increased to 100 mg/day orally
Angina Pectoris
Adult: 50 mg/day orally; after 1 week, may be increased to 100 mg/day orally; some patients
may require 200 mg/day
Geriatric: 25 mg/day orally; after 1 week, may be increased to 100 mg/day; some patients
may require 200 mg/day
Geriatric: 100 mg orally once daily or divided every 12 hours for 6-9 days after MI
Thyrotoxicosis (off-label)
25-100 mg orally once daily or divided every 12 hours
Dosage forms
Tenormin is available in 25, 50 and 100 mg strength tablets; it is also available vials of 5 mg
atenolol in ten ml of citrate-buffered solution for intravenous injection. The IV preparation
should only be administered by trained personnel. The usual dose for tablets begins at 25 mg
once or twice per day and is modified by patient response to the medication. The following
information applies to both the tablet and IV forms of atenolol.
Side effects[3,4]
Atenolol has been well tolerated by most patients. Overall profile of adverse effects of
atenolol generally resembles that of propranolol, although a smaller proportion of patients has
discontinued treatment with atenolol (2.2% versus 9.7%).
• constipation
• diarrhoea
• dizziness
• headache
• shortness of breath
• unexplained tiredness
• leg pain
If these effects are mild, they may go away within a few days or a couple of weeks. If they’re
more severe or don’t go away, then there is need of doctor’s or pharmacist’s help.
Atenolol can however, be given with caution to those with obstructive airways disease,
provided full doses of a β2-agonist bronchodilator are given at the same time. Although a
single case of retroperitoneal fibrosis has been reported in a patient receiving atenolol, a
causal relationship was not clearly established.
Atenolol in pregnency
The FDA classifies Atenolol as a Pregnancy Category D medication which means that it can
cause harm on the unborn child when used during pregnancy. Atenolol passes the placenta
which exposes the fetus to possible negative effects. In addition, some studies have shown
that taking Atenolol during second trimester of pregnancy results in infants that are smaller
for gestational age and with lower birth weight. Fetal exposure to Atenolol during the last
months of pregnancy increases the infant’s risk . Slow heart rate (bradycardia), Low blood
sugar (hypoglycemia) and Low blood pressure (hypotension) immediately or several hours
after delivery.
Atenolol is not recommended for breastfeeding women. This medication is excreted in the
human milk and can cause unwanted effects on the nursing infant.
Atenolol tends to accumulate in the breast milk. Clinical studies reveal that breast milk
contains Atenolol at a ratio of 1.5 to 6.8 when compared to drug levels in plasma.
Precautions
Cardiac failure
Sympathetic stimulation is necessary in supporting circulatory function in congestive heart
failure, and beta blockade carries the potential hazard of further depressing myocardial
contractility and precipitating more severe failure.
In patients with acute myocardial infarction, cardiac failure, which is not promptly and
effectively controlled by 80 mg of intravenous furosemide or equivalent therapy, is a
contraindication to beta blocker treatment.
Bronchospastic diseases
Patients with bronchospastic disease should not, in general, not receive beta blockers.
Because of its relative beta 1 selectivity, however, atenolol may be used with caution in
patients with bronchospastic disease who do not respond to, or cannot tolerate, other
antihypertensive treatment. Since beta 1 selectivity is not absolute, the lowest possible dose
of atenolol should be used with therapy initiated at 50 mg and a beta 2- stimulating agent
(bronchodilator) should be made available. If dosage must be increased, dividing the dose
should be considered in order to achieve lower peak blood levels.
Major surgery
Chronically administered beta-blocking therapy should not be routinely withdrawn prior to
major surgery; however the impaired ability of the heart to respond to reflex adrenergic
stimuli may augment the risks of general anesthesia and surgical procedures.
Thyrotoxicosis
Beta-adrenergic blockade may mask certain clinical signs (e.g., tachycardia) of
hyperthyroidism. Abrupt withdrawal of beta blockade might precipitate a thyroid storm;
therefore, patients suspected of developing thyrotoxicosis from whom atenolol therapy is to
be withdrawn should be monitored closely.
Untreated Pheochromocytoma
Atenolol should not be given to patients with untreated pheochromocytoma.
Table 1: Atenolol is known to interact with other drugs, the details of drug interactions
is as follows.
CONCLUSION
From the above discussion it is concluded that atenolol is very important drug for the
treatment of several disease. Atenolol belongs to beta blocker class of drugs. It is one of the
most commonly prescribed betablocker all over the world. Atenolol is a cardioselective β-
blocker, selective β1 adrenergic antagonist. Atenolol was first introduced in 1976 and has
been approved by the US FDA from August 1981 as a therapeutic agent for both
hypertension and coronary artery disease. Since itis more prescribed it have low
bioavailability which is the major problem in the action of atenolol. Which will be modified
by several methods.
REFERENCES
1. Raghavendra Kumar Gunda, J. N. Suresh Kumar, Chandan Kumar Brahma, V.
Satyanarayana, K. Naga Prashant, Design, Formulation and Evaluation of Atenolol
Gastro Retentive Floating Tablets , Asian Journal of Pharmaceutics, 2015; 9(4): 34- 42.
2. Radha Rani Earle, Lakshmi Usha. Ayalasomayajula, P. Venkatesh, P. Ganapathi Naidu,
S. Vidya Sagar, Bhagya Sree Vani, Formulation and evaluation of atenolol orodispersable
tablets by co-processed super-disintegration process, International Journal of Advances in
Pharmaceutics, 2016; 5(2): 46-51.