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Atenolol tablets are indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure lowers the risk of fatal and non-fatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including atenolol. Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise, and limited sodium intake. Many patients will require more than 1 drug to achieve blood pressure goals. For specific advice on goals and management, see published guidelines, such as those of the National High Blood Pressure Education Program's Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC). Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mech
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ATENOLOL - atenolol tablet

A-S Medication Solutions


Atenolol Tablets, USP

Rx Only


Atenolol, a synthetic, beta -selective (cardioselective) adrenoreceptor blocking agent,

may be chemically described as 4 - [2-hydroxy-3-[(1- methylethyl) amino] propoxy]-

benzeneacetamide. The molecular and structural formulas are:



Atenolol (free base) has a molecular weight of 266.34. It is a relatively polar hydrophilic

compound with a water solubility of 26.5 mg/mL at 37°C and a log partition coefficient

(octanol/water) of 0.23. It is freely soluble in 1N HCl (300 mg/mL at 25°C) and less

soluble in chloroform (3 mg/mL at 25°C).

Atenolol tabletsare available as 25, 50 and 100 mg tablets for oral administration.

Inactive Ingredients:microcrystalline cellulose, povidone, sodium starch glycolate,

colloidal silicon dioxide and magnesium stearate


Atenolol is a beta -selective (cardioselective) beta-adrenergic receptor blocking agent

without membrane stabilizing or intrinsic sympathomimetic (partial agonist) activities.

This preferential effect is not absolute, however, and at higher doses, atenolol inhibits

beta -adrenoreceptors, chieflylocated in the bronchial and vascular musculature.

Pharmacokinetics and Metabolism

In man, absorption of an oral dose is rapid and consistent but incomplete.

Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the

remainder being excreted unchanged in the feces. Peak blood levels are reached

between two (2) and four (4) hours after ingestion. Unlike propranolol or metoprolol, but

like nadolol, atenolol undergoes little or no metabolism by the liver, and the absorbed

portion is eliminated primarily by renal excretion. Over 85% of an intravenous dose is

excreted in urine within 24 hours compared with approximately 50% for an oral dose.

Atenolol also differs from propranolol in that only a small amount (6%-16%) is bound to

proteins in the plasma. This kinetic profile results in relatively consistent plasma drug

levels with about a fourfold interpatient variation.

The elimination half- life of oral atenolol is approximately 6 to 7 hours, and there is no





alteration of the kinetic profile of the drug by chronic administration. Following

intravenous administration, peak plasma levels are reached within 5 minutes. Declines

from peak levels are rapid (5- to 10-fold) during the first 7 hours; thereafter, plasma

levels decay with a half-life similar to that of orally administered drug. Following oral

doses of 50 mg or 100 mg, both beta-blocking and antihypertensive effects persist for

at least 24 hours. When renal function is impaired, elimination of atenolol is closely

related to the glomerular filtration rate; significant accumulation occurs when the

creatinine clearance falls below 35 mL/min/1.73m . (See DOSAGE AND



In standard animal or human pharmacological tests, beta- adrenoreceptor blocking

activity of Atenolol has been demonstrated by: (1) reduction in resting and exercise

heart rate and cardiac output, (2) reduction of systolic and diastolic blood pressure at

rest and on exercise, (3) inhibition of isoproterenol induced tachycardia, and (4)

reduction in reflex orthostatic tachycardia.

A significant beta-blocking effect of atenolol, as measured by reduction of exercise

tachycardia, is apparent within one hour following oral administration of a single dose.

This effect is maximal at about 2 to 4 hours, and persists for at least 24 hours.

Maximum reduction in exercise tachycardia occurs within 5 minutes of an intravenous

dose. For both orally and intravenously administered drug, the duration of action is dose

related and also bears a linear relationship to the logarithm of plasma atenolol

concentration. The effect on exercise tachycardia of a single 10 mg intravenous dose is

largely dissipated by 12 hours, whereas beta-blocking activity of single oral doses of 50

mg and 100 mg is still evident beyond 24 hours following administration. However, as

has been shown for all beta-blocking agents, the antihypertensive effect does not

appear to be related to plasma level.

In normal subjects, the beta selectivity of atenolol has been shown by its reduced ability

to reverse the beta -mediated vasodilating effect of isoproterenol as compared to

equivalent beta-blocking doses of propranolol. In asthmatic patients, a dose of

atenololproducing a greater effect on resting heart rate than propranolol resulted in

much less increase in airway resistance. In a placebo controlled comparison of

approximately equipotent oral doses of several beta blockers, atenolol produced a

significantly smaller decrease of FEV than nonselective beta blockers such as

propranolol and, unlike those agents, did not inhibit bronchodilation in response to


Consistent with its negative chronotropic effect due to beta blockade of the SA node,

atenolol increases sinus cycle length and sinus node recovery time. Conduction in the

AV node is also prolonged. Atenolol is devoid of membrane stabilizing activity, and

increasing the dose well beyond that producing beta blockade does not further depress

myocardial contractility. Several studies have demonstrated a moderate (approximately

10%) increase in stroke volume at rest and during exercise.

In controlled clinical trials, atenolol tablets, given as a single daily oral dose, was an

effective antihypertensive agent providing 24-hour reduction of blood pressure. Atenolol

tablets have been studied incombination with thiazide type diuretics, and the blood

pressure effects of the combination are approximately additive. Atenolol tabletsare also

compatible with methyldopa, hydralazine, and prazosin, each combination resulting in a

larger fall in blood pressure than with the single agents. The dose range of atenolol is

narrow and increasing the dose beyond 100 mg once daily is not associated with

increased antihypertensive effect. The mechanisms of the antihypertensive effects of

beta-blocking agents have not been established. Several possible mechanisms have

been proposed and include: (1) competitive antagonism of catecholamines at peripheral

(especially cardiac) adrenergic neuron sites, leading to decreased cardiac output, (2) a

central effect leading to reduced sympathetic outflow to the periphery, and (3)

suppression of renin activity. The results from long-term studies have not shown any

diminution of the antihypertensive efficacy of atenolol tabletswith prolonged use.

By blocking the positive chronotropic and inotropic effects of catecholamines and by

decreasing blood pressure, atenolol generally reduces the oxygen requirements of the

heart at any given level of effort, making it useful for many patients in the long-term

management of angina pectoris. On the other hand, atenolol can increase oxygen

requirements by increasing left ventricular fiber length and end diastolic pressure,

particularly in patients with heart failure.

In a multicenter clinical trial (ISIS-1) conducted in 16,027 patients with suspected

myocardial infarction, patients presenting within 12 hours (mean = 5 hours) after the

onset of pain were randomized to either conventional therapy plus atenolol tablets(n =

8,037), or conventional therapy alone (n = 7,990). Patients with a heart rate of < 50

bpm or systolic blood pressure < 100 mm Hg or with other contraindications to beta

blockade were excluded. Thirty- eight percent of each group were treated within 4 hours

of onset of pain. The mean time from onset of pain to entry was 5.0 ± 2.7 hours in both

groups. Patients in the atenololgroup were to receive Atenolol I.V. Injection 5-10 mg

given over 5 minutes plus atenolol tablets 50 mg every 12 hours orally on the first study

day (the first oral dose administered about 15 minutes after the IV dose) followed by

either atenolol tablets 100 mg once daily or atenololtablets 50 mg twice daily on days 2-

7. The groups were similar in demographic and medical history characteristics and in

electrocardiographic evidence of myocardial infarction, bundle branch block, and first

degree atrioventricular block at entry.

During the treatment period (days 0- 7), the vascular mortality rates were 3.89% in the

atenolol tablets group (313 deaths) and 4.57% in the control group (365 deaths). This

absolute difference in rates, 0.68%, is statistically significant at the P < 0.05 level. The

absolute difference translates into a proportional reduction of 15% (3.89-4.57/4.57 = -

0.15). The 95% confidence limits are 1%- 27%. Most of the difference was attributed to

mortality in days 0-1 (Atenolol - 121 deaths; control - 171 deaths).

Despite the large size of the ISIS-1 trial, it is not possible to identify clearly subgroups of

patients most likely or least likely to benefit from early treatment with atenolol. Good

clinical judgment suggests, however, that patients who are dependent on sympathetic

stimulation for maintenance of adequate cardiac output and blood pressure are not

good candidates for beta blockade. Indeed, the trial protocol reflected that judgment by

excluding patients with blood pressure consistently below 100 mm Hg systolic. The

overall results of the study are compatible with the possibility that patients with

borderline blood pressure (less than 120 mm Hg systolic), especially if over 60 years of

age, are less likely to benefit.

The mechanism through which atenolol improves survival in patients with definite or

suspected acute myocardial infarction is unknown, as is the case for other beta blockers

in the postinfarction setting. Atenolol, in addition to its effects on survival, has shown

other clinical benefits including reduced frequency of ventricular premature beats,

reduced chest pain, and reduced enzyme elevation.

Atenolol Geriatric Pharmacology:

In general, elderly patients present higher atenolol plasma levels with total clearance

values about 50% lower than younger subjects. The half-life is markedly longer in the

elderly compared to younger subjects. The reduction in atenolol clearance follows the

general trend that the elimination of renallyexcreted drugs is decreased with increasing




Atenolol tablets are indicated for the treatment of hypertension, to lower blood

pressure. Lowering blood pressure lowers the risk of fatal and non-fatal cardiovascular

events, primarily strokes and myocardial infarctions. These benefits have been seen in

controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes

including atenolol.

Control of high blood pressure should be part of comprehensive cardiovascular risk

management, including, as appropriate, lipid control, diabetes management,

antithrombotic therapy, smoking cessation, exercise, and limited sodium intake. Many

patients will require more than 1 drug to achieve blood pressure goals. For specific

advice on goals and management, see published guidelines, such as those of the

National High Blood Pressure Education Program's Joint National Committee on

Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC).

Numerous antihypertensive drugs, from a variety of pharmacologic classes and with

different mechanisms of action, have been shown in randomized controlled trials to

reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood

pressure reduction, and not some other pharmacologic property of the drugs, that is

largely responsible for those benefits. The largest and most consistent cardiovascular

outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial

infarction and cardiovascular mortality also have been seen regularly.

Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the

absolute risk increase per mmHg is greater at higher blood pressures, so that even

modest reductions of severe hypertension can provide substantial benefit. Relative risk

reduction from blood pressure reduction is similar across populations with varying

absolute risk, so the absolute benefit is greater in patients who are at higher risk

independent of their hypertension (for example, patients with diabetes or

hyperlipidemia), and such patients would be expected to benefit from more aggressive

treatment to a lower blood pressure goal.

Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in

black patients, and many antihypertensive drugs have additional approved indications

and effects (eg, on angina, heart failure, or diabetic kidney disease). These

considerations may guide selection of therapy.

Atenolol tablets may be administered with other antihypertensive agents.

Angina Pectoris Due to Coronary Atherosclerosis

Atenolol tablets are indicated for the long-term management of patients with angina


Acute Myocardial Infarction

Atenolol tablets are indicated in the management of hemodynamically stable patients

with definite or suspected acute myocardial infarction to reduce cardiovascular

mortality. Treatment can be initiated as soon as the patient's clinical condition allows.


In general, there is no basis for treating patients like those who were excluded from the

ISIS -1 trial (blood pressure less than 100 mm Hg systolic, heart rate less than 50 bpm)

or have other reasons to avoid beta blockade. As noted above, some subgroups (eg,

elderly patients with systolic blood pressure below 120 mm Hg) seemed less likely to



Atenolol tablets are contraindicated in sinus bradycardia, heart block greater than first

degree, cardiogenic shock, and overt cardiac failure. (See WARNINGS.)

Atenolol tablets are contraindicated in those patients with a history of hypersensitivity to

the atenolol or anyof the drug product's components.


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.

In Patients without a History of Cardiac Failure

Continued depression of the myocardium with beta-blocking agents over a period of

time can, in some cases, lead to cardiac failure. At the first sign or symptom of

impending cardiac failure, patients should be treated appropriately according to

currently recommended guidelines, and the response observed closely. If cardiac failure

continues despite adequate treatment, atenolol tablets should be withdrawn. (See


Cessation of Therapy with Atenolol Tablets

Patients with coronary artery disease, who are being treated with Atenolol tablets, should be advised

against abrupt discontinuation of therapy. Severe exacerbation of angina and the occurrence of

myocardial infarction and ventricular arrhythmias have been reported in angina patients following the

abrupt discontinuation of therapy with beta blockers. The last two complications may occur with or

without preceding exacerbation of the angina pectoris. As with other beta blockers, when

discontinuation of atenolol tablets is planned, the patients should be carefully observed and advised to

limit physical activity to a minimum. If the angina worsens or acute coronary insufficiency develops, it is

recommended that atenolol tablets be promptly reinstituted, at least temporarily. Because coronary

artery disease is common and may be unrecognized, it may be prudent not to discontinue atenolol

tablets therapy abruptly even in patients treated only for hypertension. (See DOSAGE AND


Concomitant Use of Calcium Channel Blockers

Bradycardia and heart block can occur and the left ventricular end diastolic pressure can

rise when beta-blockers are administered with verapamil or diltiazem. Patients with pre-

existing conduction abnormalities or left ventricular dysfunction are particularly

susceptible. (See PRECAUTIONS.)

Bronchospastic Diseases


RECEIVE BETA BLOCKERS. Because of its relative beta selectivity, however,

Atenolol tablets may be used with caution in patients with bronchospastic

disease who do not respond to, or cannot tolerate, other antihypertensive

treatment. Since beta selectivity is not absolute, the lowest possible dose

of atenolol tablets should be used with therapy initiated at 50 mg and a

beta -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.

Diabetes and Hypoglycemia

Atenolol tablets should be used with caution in diabetic patients if a beta-blocking agent

is required. Beta blockers may mask tachycardia occurring with hypoglycemia, but other

manifestations such as dizziness and sweating may not be significantly affected. At

recommended doses atenolol does not potentiate insulin-induced hypoglycemia and,

unlike nonselective beta blockers, does not delay recovery of blood glucose to normal



Beta-adrenergic blockade may mask certain clinical signs (eg, tachycardia) of

hyperthyroidism. Abrupt withdrawal of beta blockade might precipitate a thyroid storm;

therefore, patients suspected of developing thyrotoxicosis from whom atenolol tablets

therapy is to be withdrawn should be monitored closely. (See DOSAGE AND


Untreated Pheochromocytoma

Atenolol tablets should not be given to patients with untreated pheochromocytoma.

Pregnancy and Fetal Injury

Atenolol can cause fetal harm when administered to a pregnant woman. Atenolol

crosses the placental barrier and appears in cord blood. Administration of atenolol,

starting in the second trimester of pregnancy, has been associated with the birth of

infants that are small for gestational age. No studies have been performed on the use of

atenolol in the first trimester and the possibility of fetal injury cannot be excluded. If this

drug is used during pregnancy, or if the patient becomes pregnant while taking this

drug, the patient should be apprised of the potential hazard to the fetus.

Neonates born to mothers who are receiving Atenolol at parturition or breast-feeding

may be at risk for hypoglycemia and bradycardia. Caution should be exercised when

atenolol tablets is administered during pregnancy or to a woman who is breast-feeding.

(See PRECAUTIONS, Nursing Mothers.)

Atenolol has been shown to produce a dose-related increase in embryo/fetal resorptions

in rats at doses equal to or greater than 50 mg/kg/day or 25 or more times the

maximum recommended human antihypertensive dose.* Although similar effects were

not seen in rabbits, the compound was not evaluated in rabbits at doses above 25

mg/kg/day or 12.5 times the maximum recommended human antihypertensive dose.*



Patients already on a beta blocker must be evaluated carefully before Atenolol tabletsare

administered Initial and subsequent Atenolol tablet dosages can be adjusted downward

depending on clinical observations including pulse and blood pressure. Atenolol may

aggravate peripheral arterial circulatory disorders.

Impaired Renal Function

The drug should be used with caution in patients with impaired renal function. (See


*Based on the maximum dose of 100 mg/day in a 50 kg patient.

Drug Interactions

Catecholamine-depleting drugs (eg, reserpine) may have an additive effect when given

with beta-blocking agents. Patients treated with atenolol tablets plus a catecholamine

depletor should therefore beclosely observed for evidence of hypotension and/or

marked bradycardia which may produce vertigo, syncope, or postural hypotension.

Calcium channel blockers may also have an additive effect when given with atenolol

tablets (See WARNINGS).

Disopyramide is a Type I antiarrhythmic drug with potent negative inotropic and

chronotropic effects. Disopyramide has been associated with severe bradycardia,

asystole and heart failure when administered with beta blockers.

Amiodarone is an antiarrhythmic agent with negative chronotropic properties that may

be additive to those seen with beta blockers.

Beta blockers may exacerbate the rebound hypertension which can follow the

withdrawal of clonidine. If the two drugs are coadministered, the beta blocker should be

withdrawn several days before the gradual withdrawal of clonidine. If replacing clonidine

by beta-blocker therapy, the introduction of beta blockers should be delayed for several

days after clonidine administration has stopped.

Concomitant use of prostaglandin synthase inhibiting drugs, eg, indomethacin, may

decrease the hypotensive effects of beta blockers.

Information on concurrent usage of atenolol and aspirin is limited. Data from several

studies, ie, TIMI-II, ISIS-2, currently do not suggest any clinical interaction between

aspirin and beta blockers in the acute myocardial infarction setting.

While taking beta blockers, patients with a history of anaphylactic reaction to a variety of

allergens may have a more severe reaction on repeated challenge, either accidental,

diagnostic or therapeutic. Such patients may be unresponsive to the usual doses of

epinephrine used to treat the allergic reaction.

Both digitalis glycosides and beta-blockers slow atrioventricular conduction and

decrease heart rate.

Concomitant use can increase the risk of bradycardia.

Carcinogenesis, Mutagenesis, Impairment of Fertility

Two long-term (maximum dosing duration of 18 or 24 months) rat studies and one

long- term (maximum dosing duration of 18 months) mouse study, each employing

dose levels as high as 300 mg/kg/day or 150 times the maximum recommended human

antihypertensive dose,* did not indicate a carcinogenic potential of atenolol. A third (24

month) rat study, employing doses of 500 and 1,500 mg/kg/day (250 and 750 times the

maximum recommended human antihypertensive dose*) resulted in increased

incidences of benign adrenal medullary tumors in males and females, mammary

fibroadenomas in females, and anterior pituitary adenomas and thyroid parafollicular cell

carcinomas in males. No evidence of a mutagenic potential of atenolol was uncovered in

the dominant lethal test (mouse), in vivo cytogenetics test (Chinese hamster) or Ames

test (S.typhimurium).

Fertility of male or female rats (evaluated at dose levels as high as 200 mg/kg/day or 100

times the maximum recommended human dose*) was unaffected by atenolol


Animal Toxicology

Chronic studies employing oral atenolol performed in animals have revealed the

occurrence of vacuolation of epithelial cells of Brunner's glands in the duodenum of both

male and female dogs at all tested dose levels of atenolol (starting at 15 mg/kg/day or

7.5 times the maximum recommended human antihypertensive dose*) and increased

incidence of atrial degeneration of hearts of male rats at 300 but not 150 mg

atenolol/kg/day (150 and 75 times the maximum recommended human antihypertensive

dose,* respectively).

Usage in Pregnancy

Pregnancy Category D

See WARNINGS - Pregnancy and Fetal Injury.

*Based on the maximum dose of 100 mg/day in a 50 kg patient.

Nursing Mothers

Atenolol is excreted in human breast milk at a ratio of 1.5 to 6.8 when compared to the

concentration in plasma. Caution should be exercised when Atenolol tablets is

administered to a nursing woman. Clinically significant bradycardia has been reported in

breast-fed infants. Premature infants, or infants with impaired renal function, may be

more likely to develop adverse effects.

Neonates born to mothers who are receiving atenolol tabletsat parturition or breast-

feeding may be at risk for hypoglycemia and bradycardia. Caution should be exercised

when Atenolol tabletsare administered during pregnancy or to a woman who is breast-

feeding (See WARNINGS, Pregnancy and Fetal Injury).

Pediatric Use

Safety and effectiveness in pediatric patients have not been established.

Geriatric Use

Hypertension and Angina Pectoris Due to Coronary Atherosclerosis:

Clinical studies of atenolol tabletsdid not include sufficient number of patients aged 65

and over to determine whether they respond differently from younger subjects. Other

reported clinical experience has not identified differences in responses between the

elderly and younger patients. In general, dose selection for an elderly patient should be

cautious, usually starting at the low end of the dosing range, reflecting the greater

frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease

or other drug therapy.

Acute Myocardial Infarction:

Of the 8,037 patients with suspected acute myocardial infarction randomized to atenolol

in the ISIS-1 trial (See CLINICAL PHARMACOLOGY), 33% (2,644) were 65 years of

age and older. It was not possible to identify significant differences in efficacy and safety

between older and younger patients; however, elderly patients with systolic blood

pressure < 120 mmHg seemed less likely to benefit (See INDICATIONS AND USAGE).

In general, dose selection for an elderly patient should be cautious, usually starting at

the low end of the dosing range, reflecting greater frequency of decreased hepatic,

renal, or cardiac function, and of concomitant disease or other drug therapy. Evaluation

of patients with hypertension or myocardial infarction should always include assessment

of renal function.


Most adverse effects have been mild and transient.

The frequency estimates in the following table were derived from controlled studies in

hypertensive patients in which adverse reactions were either volunteered by the patient

(US studies) or elicited, eg, by checklist (foreign studies). The reported frequency of

elicited adverse effects was higher for both atenolol tabletsand placebo-treated patients

than when these reactions were volunteered. Where frequency of adverse effects of

atenolol tabletsand placebo is similar, causal relationship to atenolol tabletsis uncertain.


(US Studies)

Total volunteered and


(Foreign + US studies)











Cold Extremities

Postural Hypotension

Leg Pain


















Acute Myocardial Infarction

In a series of investigations in the treatment of acute myocardial infarction, bradycardia

and hypotension occurred more commonly, as expected for any beta blocker, in

atenolol-treated patients than in control patients. However, these usually responded to

atropine and/or to withholding further dosage of atenolol. The incidence of heart failure

was not increased by atenolol. Inotropic agents were infrequently used. The reported

frequency of these and other events occurring during these investigations is given in the

following table.

In a study of 477 patients, the following adverse events were reported during either

intravenous and/or oral atenolol administration:

Conventional Therapy

Conventional Therapy

Plus Atenolol













Heart Failure



Heart Block



BBB + Major Axis Deviation



Supraventricular Tachycardia



Atrial Fibrillation



Atrial Flutter



Ventricular Tachycardia



Cardiac Reinfarction



Total Cardiac Arrests



Nonfatal Cardiac Arrests






Cardiogenic Shock



Development of Ventricular

Septal Defect



Development of Mitral




Renal Failure



Pulmonary Emboli



In the subsequent International Study of Infarct Survival (ISIS-1) including over 16,000

patients of whom 8,037 were randomized to receive atenolol tabletstreatment, the

dosage of intravenous and subsequent oral atenolol tabletswas either discontinued or

reduced for the following reasons:

Reasons for reduced Dosage

IV Atenolol

Reduced Dose

(<5 mg)

Oral Partial Dose

Hypotension/ Bradycardia




Cardiogenic Shock






Cardiac Arrest



Heart Block (> first




Cardiac Failure









During postmarketing experience with atenolol tablets, the following have been reported

in temporal relationship to the use of the drug: elevated liver enzymes and/or bilirubin,

hallucinations, headache, impotence, Peyronie's disease, postural hypotension which

may be associated with syncope, psoriasiform rash or exacerbation of psoriasis,

psychoses, purpura, reversible alopecia, thrombocytopenia, visual disturbance, sick

sinus syndrome, and dry mouth. Atenolol tablets, like other beta blockers, have been

associated with the development of antinuclear antibodies (ANA), lupus syndrome, and

Raynaud's phenomenon.


In addition, a variety of adverse effects have been reported with other beta-adrenergic

blocking agents, and may be considered potential adverse effects of atenolol tablets.

Hematologic: Agranulocytosis.

Full dosage was 10 mg and some patients received less than 10 mg but more than 5 mg.

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