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Atenolol is used for the management of hypertension, angina, and acute myocardial infarction (MI). The drug also has been used for the management of supraventricular and ventricular tachyarrhythmias, management of acute alcohol withdrawal (in conjunction with a benzodiazepine), and prophylaxis of migraine headache.

The choice of a β-adrenergic blocking agent (β-blocker) depends on numerous factors, including pharmacologic properties (e.g., relative β-selectivity, intrinsic sympathomimetic activity, membrane-stabilizing activity, lipophilicity), pharmacokinetics, intended use, and adverse effect profile, as well as the patient's coexisting disease states or conditions, response, and tolerance. While specific pharmacologic properties and other factors may appropriately influence the choice of a β-blocker in individual patients, evidence of clinically important differences among the agents in terms of overall efficacy and/or safety is limited. Patients who do not respond to or cannot tolerate one β-blocker may be successfully treated with a different agent.

In the management of hypertension or chronic stable angina pectoris in patients with chronic obstructive pulmonary disease (COPD) or type 1 diabetes mellitus, many clinicians prefer to use low dosages of a β1-selective adrenergic blocking agent (e.g., atenolol, metoprolol), rather than a nonselective agent (e.g., nadolol, pindolol, propranolol, timolol). However, selectivity of these agents is relative and dose dependent. Some clinicians also will recommend using a β1-selective agent or an agent with intrinsic sympathomimetic activity (ISA) (e.g., pindolol), rather than a nonselective agent, for the management of hypertension or angina pectoris in patients with peripheral vascular disease, but there is no evidence that the choice of β-blocker substantially affects efficacy.


Atenolol is used alone or in combination with other classes of antihypertensive agents in the management of hypertension. Atenolol's efficacy in hypertensive patients is similar to that of other β-blockers.

Current evidence-based practice guidelines for the management of hypertension in adults generally recommend the use of 4 classes of antihypertensive agents (angiotensin-converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, and thiazide diuretics). Although β-blockers were previously considered a drug of choice for the initial management of hypertension, most current guidelines no longer recommend these drugs as first-line therapy because of the lack of established superiority over other recommended drug classes and at least one study demonstrating that they may be less effective than angiotensin II receptor antagonists in preventing cardiovascular death, MI, or stroke. However, β-blockers may still be considered in hypertensive patients who have a compelling indication (e.g., prior MI, ischemic heart disease, heart failure) for their use or as add-on therapy in those who do not respond adequately to the preferred drug classes. Ultimately, choice of antihypertensive therapy should be individualized, considering the clinical characteristics of the patient (e.g., age, ethnicity/race, comorbid conditions, cardiovascular risk factors) as well as drug-related factors (e.g., ease of administration, availability, adverse effects, costs). Because many patients eventually will need drugs from 2 or more antihypertensive classes, experts generally state that the emphasis should be placed on achieving appropriate blood pressure control rather than on identifying a preferred drug to achieve that control.

Considerations in Initiating Antihypertensive Therapy

Drug therapy generally is reserved for patients who respond inadequately to nondrug therapy (i.e., lifestyle modifications such as diet [including sodium restriction and adequate potassium and calcium intake], regular aerobic physical activity, moderation of alcohol consumption, and weight reduction) or in whom the degree of blood pressure elevation or coexisting risk factors requires more prompt or aggressive therapy; however, the optimum blood pressure threshold for initiating antihypertensive drug therapy and specific treatment goals remain controversial.

While the Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) recommended antihypertensive drug therapy in all patients with systolic/diastolic blood pressure of 140/90 mm Hg or higher who fail to respond to lifestyle/behavioral modifications, other experts, including the panel members appointed to the Eighth Joint National Committee (JNC 8 expert panel) currently recommend a higher systolic blood pressure threshold for older individuals (e.g., the JNC 8 expert panel recommends a threshold of 150 mm Hg for patients 60 years of age or older).

In addition, there is some variation in the blood pressure thresholds and treatment goals recommended for patients with diabetes mellitus or chronic kidney disease. In the past, initial antihypertensive drug therapy was recommended for patients with diabetes mellitus or chronic kidney disease who had blood pressures of 130/80 mm Hg or higher; however, current hypertension management guidelines generally recommend the same blood pressure threshold of 140/90 mm Hg for initiating antihypertensive drug therapy in these individuals as for the general population of patients without these conditions, although a lower goal (e.g., less than 130/80 mm Hg) may still be considered.

Further study is needed to more clearly define optimum blood pressure goals in patients with hypertension; when determining appropriate blood pressure goals, individual risks and benefits should be considered in addition to the evidence from clinical studies.

Antihypertensive drug therapy generally should be initiated gradually and titrated at intervals of approximately 2-4 weeks to achieve the target blood pressure. The goal is to reduce blood pressure to levels below the threshold used for initiating drug therapy. Addition of a second drug should be initiated when use of monotherapy in adequate dosages fails to achieve goal blood pressure. Some experts state that initial antihypertensive therapy with a combination of drugs may be considered in patients with systolic/diastolic blood pressure greater than 20/10 mm Hg above goal blood pressure. Such combined therapy may increase the likelihood of achieving goal blood pressure in a more timely fashion, but also may increase the risk of adverse effects (e.g., orthostatic hypotension) in some patients (e.g., elderly). Initial combined therapy may be particularly useful in patients with markedly high baseline blood pressures and those with additional risk factors.

Initial Drug Therapy

For initial antihypertensive drug therapy, experts currently recommend a thiazide diuretic, calcium-channel blocker, ACE inhibitor, or angiotensin II receptor antagonist. β-Blockers generally are not preferred for initial monotherapy in patients with uncomplicated hypertension, but may be beneficial in patients with a compelling indication (e.g., ischemic heart disease, atrial tachyarrhythmias, history of MI, heart failure) for their use.

Follow-up and Maintenance Therapy

Several strategies are recommended for the titration and combination of antihypertensive drugs; these strategies include maximizing the dosage of the first drug before adding a second drug, adding a second drug before achieving maximum dosage of the initial drug, or initiating therapy with 2 drugs simultaneously (either as separate preparations or as a fixed-dose combination). If goal blood pressure is not achieved with initial monotherapy with one of the recommended antihypertensive drug classes, a second drug from one of the recommended drug classes may be added; if goal blood pressure is not achieved with optimal dosages of 2 antihypertensive agents, a third antihypertensive agent from one of the recommended drug classes may be added. If more than 3 drugs are required, other antihypertensive drug classes, including β-blockers, may be considered. If the blood pressure goal cannot be achieved with the above recommended strategies, consultation with a hypertension specialist should be considered.

Thus, atenolol can be used for the management of hypertension as initial monotherapy (not usually preferred, but may be used in patients with a compelling indication) or as a component of a multiple-drug regimen. β-Blockers often are used concurrently with a diuretic because of their additive effects. β-Blockers also have been combined with vasodilators (e.g., hydralazine, minoxidil) to counteract the reflex tachycardia that occurs with vasodilators.

Antihypertensive Therapy for Patients with Underlying Cardiovascular or Other Risk Factors

Drug therapy in patients with hypertension and underlying cardiovascular or other risk factors should be carefully individualized based on the underlying disease(s), concomitant drugs, tolerance to drug-induced adverse effects, and blood pressure goal.

Ischemic Heart Disease

The selection of an appropriate antihypertensive agent in patients with ischemic heart disease should be based on individual patient characteristics, but may include a β-blocker, with the addition of other drugs (e.g., ACE inhibitors, thiazide diuretics, calcium-channel blockers) as necessary to achieve blood pressure goals. Because of the demonstrated mortality benefit of β-blockers following MI, these drugs should be administered in all patients who have survived an MI.

Heart Failure

While β-blockers as single therapies are not superior to other antihypertensive agents in the reduction of all cardiovascular outcomes, certain β-blockers have been shown to be effective in reducing the incidence of heart failure and associated morbidity and mortality.

Other Special Considerations for Antihypertensive Therapy


In general, black hypertensive patients tend to respond better to monotherapy with thiazide diuretics or calcium-channel blocking agents than to monotherapy with β-blockers, ACE inhibitors, or angiotensin II receptor antagonists. However, such diminished response to a β-blocker is largely eliminated when the drug is administered concomitantly with a thiazide diuretic. In addition, some experts state that when use of β-blockers is indicated in hypertensive patients with underlying cardiovascular or other risk factors, these indications should be applied equally to black hypertensive patients.

For information on overall principles and expert recommendations for treatment of hypertension, see Uses: Hypertension in Adults in the Thiazides General Statement 40:28.20.

Chronic Stable Angina

Atenolol is used for the management of chronic stable angina pectoris. β-Blockers are recommended as the anti-ischemic drugs of choice in most patients with chronic stable angina; despite differences in cardioselectivity, intrinsic sympathomimetic activity, and other clinical factors, all β-blockers appear to be equally effective for this indication. Long-term use of β-blockers in patients with chronic stable angina pectoris has been shown to reduce the frequency of anginal attacks, allow a reduction in nitroglycerin dosage, and increase exercise tolerance.

Combination therapy with a β-blocker and a nitrate appears to be more effective than either drug alone because β-blockers attenuate the increased sympathetic tone and reflex tachycardia associated with nitrate therapy while nitrate therapy (e.g., nitroglycerin) counteracts the potential increase in left-ventricular wall tension associated with a decrease in heart rate. Combined therapy with a β-blocker and a dihydropyridine calcium-channel blocker also may be useful because the tendency to develop tachycardia with the calcium-channel blocker is counteracted by the β-blocker. However, caution should be exercised in the concomitant use of β-blockers and the nondihydropyridine calcium-channel blockers verapamil or diltiazem because of the potential for excessive fatigue, bradycardia, or atrioventricular (AV) block.(See Drug Interactions: Cardiovascular Drugs.)

Non-ST-Segment-Elevation Acute Coronary Syndromes

β-Blockers are used as part of the standard therapeutic measures for managing non-ST-segment-elevation acute coronary syndromes (NSTE ACS). Patients with NSTE ACS have either unstable angina or non-ST-segment-elevation MI (NSTEMI); because these conditions are part of a continuum of acute myocardial ischemia and have indistinguishable clinical features upon presentation, the same initial treatment strategies are recommended. The American Heart Association/American College of Cardiology (AHA/ACC) guideline for the management of patients with NSTE ACS recommends an early invasive strategy (angiographic evaluation with the intent to perform revascularization procedures such as percutaneous coronary intervention [PCI] with coronary artery stent implantation or coronary artery bypass grafting [CABG]) or an ischemia-guided strategy (initial medical management followed by cardiac catheterization and revascularization if indicated) in patients with definite or likely NSTE ACS; standard medical therapies for all patients should include a β-blocker, antiplatelet agents (aspirin and/or a P2Y12-receptor antagonist), anticoagulant agents (e.g., low molecular weight or unfractionated heparin), nitrates (e.g., nitroglycerin), and analgesic agents regardless of the initial management approach. The guideline states that oral β-blocker therapy should be initiated within the first 24 hours in patients who do not have manifestations of heart failure, evidence of a low-output state, increased risk of cardiogenic shock, or any other contraindications to β-blocker therapy; use of IV β-blockers is potentially harmful in patients with risk factors for cardiogenic shock. Continued therapy with a β-blocker proven to reduce mortality (bisoprolol, carvedilol, or metoprolol succinate) is recommended in patients with stabilized heart failure and reduced systolic function.

Acute Myocardial Infarction

Atenolol is used to reduce the risk of cardiovascular mortality in hemodynamically stable patients with definite or suspected acute MI. The term MI is used when there is evidence of myocardial necrosis in the setting of acute myocardial ischemia. ST-segment-elevation MI (STEMI) is distinguished from NSTEMI based on the presence or absence of ST-segment elevation on ECG. Patients with STEMI typically have complete arterial occlusion; therefore, immediate reperfusion therapy (with primary PCI or thrombolytic agents) is the current standard of care for such patients. Because the clinical presentation of NSTEMI is similar to that of unstable angina, these conditions are considered together in current expert guidelines.(See Uses: Non-ST-Segment-Elevation Acute Coronary Syndromes.) During the early stage of a definite or suspected MI, atenolol has been initiated with IV doses (no longer commercially available in the US), followed by continued oral dosing; however, experts currently recommend that early IV use of β-blockers be limited to selected patients.

Because β-blockers can reduce myocardial oxygen demand during the first few hours of an acute MI by reducing heart rate, arterial blood pressure, and myocardial contractility, and also have been shown to reduce mortality, early IV therapy with these drugs was routinely recommended following acute MI. Evidence supporting this recommendation was generally based on studies conducted prior to the reperfusion era demonstrating a reduction in mortality and other clinical benefits (i.e., reduced infarct size, incidence of ventricular arrhythmias, chest pain, and cardiac enzyme elevations) with early use of β-blockers during MI. In one such study (the First International Study of Infarct Survival; ISIS-1), therapy with atenolol (initiated IV within the first 12 hours of symptom onset and continued orally for 7 days) was shown to reduce cardiovascular mortality by approximately 15% during the first few days of therapy, but did not substantially reduce cardiovascular mortality beyond this initial period. The difference in vascular mortality rate between those receiving atenolol or placebo was evident almost entirely during the first 2 days of therapy. Analysis of data from a subset of patients who died during early treatment in ISIS-1 suggested that the principal mechanism of early mortality reduction associated with atenolol therapy was prevention of cardiac rupture and of cardiac electromechanical dissociation. However, the relevance of these study findings to current clinical practice has been questioned since patients did not receive reperfusion therapy and only 5% received an antiplatelet agent.

Studies conducted after the widespread use of reperfusion therapy generally have demonstrated more attenuated benefits with early β-blocker therapy in patients with acute MI; while β-blockers may still confer benefits (e.g., reduction in the risk of reinfarction and ventricular arrhythmias), there is less certainty regarding the drugs' effects on mortality in patients receiving contemporary revascularization and pharmacologic therapies (antiplatelet agents, ACE inhibitors, and lipid-lowering therapies). In addition, early use of β-blockers (particularly when administered IV) has been associated with an increased risk of cardiogenic shock. Based on the currently available evidence, the American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guideline for the management of STEMI recommends oral β-blocker therapy in all patients who do not have manifestations of heart failure, evidence of a low-output state, increased risk of cardiogenic shock, or any other contraindications to β-blocker therapy. Such therapy should be initiated within the first 24 hours following acute MI and continued during and after hospitalization. Because of conflicting evidence of benefit and the potential for harm, the guidelines recommend limiting use of IV β-blockers to patients with refractory hypertension or ongoing ischemia.

Although the efficacy of atenolol in reducing cardiovascular mortality has been established only during the first 7 days after an acute MI, the benefits of long-term β-blocker therapy for secondary prevention have been well established in numerous clinical studies. Patients with MI complicated by heart failure, left ventricular dysfunction, or ventricular arrhythmias appear to derive the most benefit from long-term β-blocker therapy. Data from studies using other β-blockers suggest that optimum benefit may be achieved if treatment with these agents is continued for at least 1-3 years if not indefinitely after infarction unless contraindicated. Several large, randomized studies have demonstrated that prolonged oral therapy with a β-blocker can reduce the rates of reinfarction and mortality (e.g., sudden and nonsudden cardiac death) following acute MI. It is estimated that such therapy could result in a relative reduction in mortality of about 25% annually for years 1-3 after infarction, with high-risk patients exhibiting the greatest potential benefit; the benefit of continued therapy may persist for at least several years beyond this period, although less substantially. Therefore, atenolol, like other β-blockers, can be used for secondary prevention following acute MI to reduce the risk of reinfarction and mortality. The AHA/ACCF secondary prevention guideline recommends β-blocker therapy in all patients with left ventricular systolic dysfunction (ejection fraction of 40% or less) and a prior MI; use of a β-blocker with proven mortality benefit (bisoprolol, carvedilol, or metoprolol succinate) is recommended. Although the benefits of long-term β-blockade in post-MI patients with normal left ventricular function are less well established, the guideline recommends continued β-blocker therapy for at least 3 years in such patients. Further studies are needed to establish the optimal duration of β-blocker therapy for secondary prevention of MI.

Supraventricular Arrhythmias

β-Blockers, including atenolol, have been used to slow ventricular rate in patients with supraventricular tachycardia (SVT). The American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) guideline for the management of adult patients with supraventricular tachycardia recommends the use of β-adrenergic blocking agents in the treatment of various SVTs (e.g., atrial flutter, junctional tachycardia, focal atrial tachycardia, atrioventricular nodal reentrant tachycardia [AVNRT]); in general, an IV β-blocker is recommended for acute treatment, while an oral preparation is recommended for ongoing management of these arrhythmias. Vagal maneuvers and/or IV adenosine are considered first-line interventions for the acute treatment of patients with SVT and should be attempted prior to other therapies when clinically indicated; if such measures are ineffective or not feasible, an IV β-blocker may be considered in hemodynamically stable patients. Although evidence of efficacy is limited, experts state that the overall safety of β-adrenergic blockers warrants their use in patients with SVT. Patients should be closely monitored for hypotension and bradycardia during administration of these drugs.

Atrial Fibrillation and Flutter

β-Blockers are recommended as one of several drug therapy options for ventricular rate control in patients with nonpreexcited atrial fibrillation or flutter. For acute treatment of atrial fibrillation or flutter, an IV β-adrenergic blocking agent (e.g., esmolol, propranolol, metoprolol) may be used for ventricular rate control in patients without preexcitation; an oral β-blocker such as atenolol may be used for ongoing rate control in such patients. Choice of a specific β-blocker should be individualized based on the patient's clinical condition.

Atrial Tachycardia

IV β-blockers may be used for the treatment of patients with hemodynamically stable focal atrial tachycardia (i.e., regular SVT arising from a localized atrial site), and an oral β-blocker may be used for ongoing management. Multifocal atrial tachycardia, characterized by a rapid, irregular rhythm with at least 3 distinct P-wave morphologies, is commonly associated with an underlying condition (e.g., pulmonary, coronary, or valvular heart disease) and is generally not responsive to antiarrhythmic drug therapy. Antiarrhythmic drug therapy usually is reserved for patients who do not respond to initial attempts at correcting or managing potential precipitating factors (e.g., exacerbation of chronic obstructive pulmonary disease or congestive heart failure, hypoxemia, anemia) or in whom a precipitating factor cannot be identified.

Paroxysmal Supraventricular Tachycardia

IV β-blockers may be used for the acute treatment of hemodynamically stable patients with paroxysmal supraventricular tachycardia (PSVT), including AVNRT, that is uncontrolled or unconverted by vagal maneuvers and adenosine; an oral β-blocker may be used for the ongoing management of such patients who are not candidates for, or prefer not to undergo, catheter ablation.

Junctional Tachycardia

β-Blockers are considered one of several drug therapy options that may be used for the treatment of junctional tachycardia (i.e., nonreentrant SVT originating from the AV junction), a rapid, occasionally irregular, narrow-complex tachycardia. While evidence is limited, there is some data indicating that β-blockers (specifically propranolol) are modestly effective in terminating and/or reducing the incidence of junctional tachycardia.

Ventricular Arrhythmias

β-Blockers also have been used in patients with cardiac arrest precipitated by ventricular fibrillation or pulseless ventricular tachycardia. However, AHA states that routine administration of β-blockers after cardiac arrest is potentially harmful (e.g., may worsen hemodynamic instability, exacerbate heart failure, or cause bradyarrhythmias) and is therefore not recommended.

β-Blockers may be useful in the management of certain forms of polymorphic ventricular tachycardia (e.g., associated with acute ischemia).

Vascular Headache


Atenolol has been used for the prophylaxis of migraine headache. When used prophylactically, atenolol can prevent migraine or reduce the number of attacks in some patients. However, the US Headache Consortium states that the quality of evidence for atenolol is not as compelling as it is for propranolol for this indication. Atenolol is not recommended for the treatment of a migraine attack that has already started. For further information on management and classification of migraine headache,

Alcohol Withdrawal

Atenolol has been used in conjunction with a benzodiazepine in the management of acute alcohol withdrawal. β-Blockers such as atenolol appear to be effective in reducing manifestations of the hyperadrenergic state associated with alcohol withdrawal, including elevated blood pressure, increased heart rate, and anxiety. However, β-blockers have not been shown to prevent delirium or seizures, and such drugs should be used only as adjuncts to benzodiazepines (not as monotherapy) for the treatment of alcohol withdrawal. Some clinicians state that the use of β-blockers may be particularly helpful in patients with certain coexisting conditions (e.g., coronary artery disease).

Dosage and Administration


Atenolol is administered orally; the drug also has been administered by IV injection, however a parenteral preparation no longer is commercially available in the US.

Oral administration of atenolol more frequently than once daily for the management of hypertension usually is not necessary. If atenolol is used in patients with bronchospastic disorders, therapy should be initiated cautiously; concomitant administration of a β2-adrenergic agonist and twice-daily dosing of atenolol may minimize the risk of bronchospasm in some patients.


Dosage of atenolol must be individualized and adjusted according to the patient's response and tolerance. If atenolol therapy is to be discontinued, dosage of the drug should be reduced gradually over a period of about 2 weeks.(See Cautions: Precautions and Contraindications.)


Atenolol Therapy

The panel members appointed to the Eighth Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 8 expert panel) state that evidence-based dosing information (i.e., dosages shown in randomized controlled trials to reduce complications of hypertension) should be used when available to determine target dosages of antihypertensive agents. Based on such information, an initial adult atenolol dosage of 25-50 mg once daily and a target dosage of 100 mg once daily are recommended.

The manufacturer recommends an initial adult atenolol dosage of 50 mg once daily, either alone or in combination with diuretic therapy; the full antihypertensive effect may not be evident for 1-2 weeks. If response is inadequate after a sufficient trial at the initial dosage, the manufacturer states that dosage should be increased to 100 mg once daily. Some experts state that the usual adult dosage range for treatment of hypertension is 25-100 mg daily. Dosages exceeding 100 mg daily usually do not result in further improvement in blood pressure control.

In general, antihypertensive drug therapy should be initiated at a dosage lower than the target dosage to minimize the risk of adverse effects; dosage should then be titrated upward until the effective dosage is achieved. Blood pressure should be monitored regularly during therapy and, if necessary, dosage of the antihypertensive drug adjusted accordingly. In patients who experience intolerable adverse effects with atenolol, dosage reduction should be considered; if adverse effects worsen or fail to resolve, it may be necessary to discontinue the β-adrenergic blocking agent (β-blocker) and initiate another class of antihypertensive agent. Target dosages of antihypertensive agents generally can be achieved within 2-4 weeks, but it may take up to several months.

If atenolol is used for the management of hypertension in children, some experts recommend a usual initial oral dosage of 0.5-1 mg/kg daily given as a single dose or in 2 divided doses. Dosage may be increased as necessary to a maximum dosage of 2 mg/kg (up to 100 mg) daily given as a single dose or in 2 divided doses. For information on overall principles and expert recommendations for treatment of hypertension in pediatric patients,

Atenolol/Chlorthalidone Fixed-combination Therapy

When combination therapy is required, commercially available preparations containing atenolol in combination with chlorthalidone should not be used initially. Dosage should first be adjusted by administering each drug separately. If it is determined that the optimum maintenance dosage corresponds to the ratio in the commercial combination preparation, such a preparation may be used. If the fixed-combination preparation is used, the manufacturer recommends an initial dosage of 50 mg of atenolol and 25 mg of chlorthalidone once daily. If an optimal response is not achieved, the fixed-combination preparation containing 100 mg of atenolol and 25 mg of chlorthalidone may be used once daily.

Blood Pressure Monitoring and Treatment Goals

Careful monitoring of blood pressure during initial titration or subsequent upward adjustment in dosage of atenolol is recommended.

The goal of hypertension management and prevention is to achieve and maintain optimal control of blood pressure; specific target levels of blood pressure should be individualized based on consideration of multiple factors, including patient age and comorbidities, and the currently available evidence from clinical studies.(See Hypertension: Considerations in Initiating Antihypertensive Therapy, in Uses.)

For additional information on initiating and adjusting atenolol dosage in the management of hypertension, .

Chronic Stable Angina

For the management of chronic stable angina pectoris, the initial adult oral dosage of atenolol is 50 mg once daily. If an optimum response is not achieved within one week, oral dosage should be increased to 100 mg once daily. Some patients may require an oral atenolol dosage of 200 mg once daily for optimum effect. Dosage of β-blockers in angina pectoris usually is adjusted according to clinical response and to maintain a resting heart rate of 55-60 beats/minute. Control of angina pectoris over a 24-hour period with once-daily dosing of atenolol is achieved by the use of doses larger than those necessary to achieve an immediate maximum effect. The maximum early effect on exercise tolerance occurs with oral atenolol doses of 50-100 mg, but the effect at 24 hours is attenuated at these doses, averaging about 50-75% of that observed with once-daily oral doses of 200 mg.

Acute Myocardial Infarction

Early Treatment

Atenolol therapy may be initiated as soon as possible after an acute myocardial infarction (MI) when the patient's hemodynamic condition has stabilized. During the early stage of a definite or suspected MI, atenolol has been initiated with IV doses, followed by continued oral dosing; however, a parenteral preparation of atenolol is no longer commercially available in the US. When IV dosing is excluded, atenolol can be administered orally at a dosage of 50 mg twice daily or 100 mg once daily for at least 7 days.

The American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guideline for the management of ST-segment-elevation MI (STEMI) recommends initiation of oral β-blocker therapy within the first 24 hours of an acute MI in all patients who do not have manifestations of heart failure, evidence of a low-output state, increased risk of cardiogenic shock, or any other contraindications to β-blocker therapy.

Long-term Secondary Prevention

The optimal duration of β-blocker therapy following MI remains to be clearly established. Experts generally recommend that such therapy be continued long-term in post-MI patients with left ventricular systolic dysfunction, and for at least 3 years in those with normal left ventricular function.

Supraventricular Arrhythmias

For the ongoing treatment of various supraventricular tachycardias (SVTs) (e.g., atrial flutter, atrial tachycardia, junctional tachycardia) or atrial fibrillation after initial IV therapy in adults, some experts recommend an initial oral atenolol dose of 25-50 mg daily and usual maintenance dosage of 25-100 mg daily.

Vascular Headaches


Although oral dosage of atenolol for the prophylaxis of migraine in adults has not been established, the usual effective dosage of the drug in clinical studies was 100 mg daily.

Dosage in Renal Impairment

In patients with impaired renal function, doses and/or frequency of administration of atenolol must be modified in response to the degree of renal impairment. Because decreased renal function is a physiologic consequence of aging, the possibility that modification of atenolol dosage may be necessary in geriatric patients should be considered. Initiation of oral atenolol therapy at 25 mg daily may be necessary in some renally impaired or geriatric patients being treated for hypertension; if this dosage is employed, measurement of blood pressure just prior to a dose is recommended to ensure persistence of adequate blood pressure reduction. Although similar, low-dose initial therapy may be warranted for other conditions, data currently are not available.

A maximum oral atenolol dosage of 50 mg daily is recommended for patients with creatinine clearances of 15-35 mL/minute per 1.73 m; 25 mg daily or 50 mg every other day is recommended when creatinine clearance is less than 15 mL/minute per 1.73 m. In patients undergoing hemodialysis, a 25- or 50-mg oral dose of atenolol may be administered after each dialysis; since marked reductions in blood pressure may occur, it is recommended that the supplemental dose be given under careful supervision.


Atenolol shares the toxic potentials of β-adrenergic blocking agents (β-blockers). In therapeutic dosage, atenolol usually is well tolerated and has a low incidence of adverse effects. The incidence and severity of adverse reactions may occasionally be obviated by a reduction in dosage. Abrupt withdrawal of the drug should be avoided, especially in patients with coronary artery disease, since it may exacerbate angina or precipitate myocardial infarction (MI).

Cardiovascular Effects

Potentially serious adverse cardiovascular effects of atenolol include bradycardia, which occurs in 3% of patients; profound hypotension; second- or third-degree atrioventricular (AV) block; and precipitation of severe heart failure, which is more likely to occur in patients with preexisting left ventricular dysfunction. Sick sinus syndrome has been reported during postmarketing experience in patients receiving atenolol-containing therapy. Atenolol-containing therapy is not recommended for use in patients with untreated pheochromocytoma. Bradycardia and hypotension usually can be reversed with an antimuscarinic agent like IV atropine. Isoproterenol or a transvenous cardiac pacemaker may be required for AV block. Other adverse cardiovascular effects include coldness of the extremities, reportedly occurring in 0-12% of patients; postural hypotension (which may be associated with syncope), in 2-4% of patients; and leg pain, in 0-3% of patients. When IV and oral atenolol were used in the early post-MI infarction period (for up to 10 days after onset of symptoms) in clinical trials, the principal adverse effects were bradycardia and hypotension, which occurred in up to 25% of patients receiving the drug (often combined with other therapy) and required reduction in dosage or discontinuance of atenolol in many patients. In addition, analysis of data from a subset of patients who died during early treatment in the First International Study of Infarct Survival (ISIS-1) revealed evidence of a small but not statistically significant increase in early death secondary to bradycardia and shock associated with atenolol therapy, but this potential adverse effect was outweighed substantially by beneficial effects of the drug on reduction of mortality from other causes. Atenolol may aggravate peripheral arterial circulatory disorders.

CNS Effects

Adverse CNS effects of atenolol include dizziness, fatigue, and mental depression. Lethargy, drowsiness, unusual dreams, lightheadedness, and vertigo usually occur in less than 3% of patients. Headache and hallucinations also have been reported in patients receiving atenolol. Adverse CNS effects seen with other β-blockers that may occur with atenolol include visual disturbances, disorientation, short-term memory impairment, emotional lability, psychoses, catatonia, and impaired performance on neuropsychometric tests.

GI Effects

Adverse GI reactions include diarrhea and nausea, which reportedly occur in 2-4% of patients receiving atenolol. A few cases of mesenteric arterial thrombosis and ischemic colitis have been reported in patients receiving other β-blockers. Dry mouth also has been reported in patients receiving atenolol.

Endocrine Effects

Results of a large prospective cohort study of nondiabetic adults 45-64 years of age indicate that use of β-blockers in hypertensive patients is associated with increased risk (about 28%) of developing type 2 diabetes mellitus compared with hypertensive patients who were not receiving hypotensive therapy. In this study, the number of new cases of diabetes per 1000 person-years was 33.6 or 26.3 in patients receiving a β-blocker or no drug therapy, respectively. The association between the risk of developing diabetes mellitus and use of β-blockers reportedly was not confounded by weight gain, hyperinsulinemia, or differences in heart rate. It is not known if the risk of developing type 2 diabetes is affected by β-receptor selectivity. Further studies are needed to determine whether concomitant use of ACE inhibitors (which may improve insulin sensitivity) would abrogate β-blocker-induced adverse effects related to glucose intolerance. Therefore, until results of such studies are available, the proven benefits of β-blockers in reducing cardiovascular events in hypertensive patients must be weighed carefully against the possible risks of developing type 2 diabetes mellitus.

Hypoglycemia, which may result in loss of consciousness, also may occur in nondiabetic patients receiving β-blockers. Patients most at risk for the development of β-blocker-induced hypoglycemia are those undergoing dialysis, prolonged fasting, or severe exercise regimens.

β-Blockers may mask signs and symptoms of hypoglycemia (e.g., palpitation, tachycardia, tremor) and potentiate insulin-induced hypoglycemia. Although it has been suggested that nonselective β-blockers are more likely to induce hypoglycemia than selective β-blockers, such an adverse effect also has been reported with selective β-blocking agents (e.g., atenolol). In addition, selective β-blockers are less likely to mask symptoms of hypoglycemia or delay recovery from insulin-induced hypoglycemia than nonselective β-blockers because of their vascular sparing effects; however, selective β-blockers can decrease insulin sensitivity by approximately 15-30%, which may result in increased insulin requirements.

Other Adverse Effects

Wheezing and dyspnea have occurred in patients receiving atenolol and are more likely to occur when dosage of the drug exceeds 100 mg daily. Rashes (which may be psoriasiform), exacerbation of psoriasis, lupus syndrome, drying of the eyes, visual disturbances, reversible alopecia, Peyronie's disease, antinuclear antibodies (ANA), impotence, elevated serum concentrations of hepatic enzymes and bilirubin, purpura, and thrombocytopenia also have been reported with atenolol.

The possibility that other adverse effects associated with other β-blockers may occur during atenolol therapy should be considered. These include hematologic reactions (e.g., agranulocytosis, nonthrombocytopenic or thrombocytopenic purpura); allergic reactions characterized by fever, sore throat, laryngospasm, and respiratory distress; Raynaud's phenomenon; conjunctivitis sicca; otitis; sclerosing serositis; and erythematous rash.

Precautions and Contraindications

Atenolol shares the toxic potentials of β-blockers, and the usual precautions of these agents should be observed. When atenolol is used as a fixed-combination preparation that includes chlorthalidone, the cautions, precautions, and contraindications associated with thiazide diuretics must be considered in addition to those associated with atenolol.

In patients with heart failure, sympathetic stimulation is vital for the support of circulatory function. Atenolol should be used with caution in patients with inadequate cardiac function, since heart failure may be precipitated by blockade of β-adrenergic stimulation when atenolol therapy is administered. In addition, in patients with latent cardiac insufficiency, prolonged β-adrenergic blockade may lead to cardiac failure. Although β-blockers should be avoided in patients with overt heart failure, atenolol may be administered cautiously, if necessary, to patients with well-compensated heart failure (e.g., those controlled with cardiac glycosides and/or diuretics). Patients receiving atenolol therapy should be instructed to consult their physician at the first sign or symptom of impending cardiac failure and should be adequately treated (e.g., with a cardiac glycoside and/or diuretic) and observed closely; if cardiac failure continues, atenolol should be discontinued, gradually if possible. In patients with acute MI, use of atenolol is contraindicated in those whose congestive heart failure cannot be controlled promptly and effectively with a parenteral loop diuretic or comparable therapy. In addition, good clinical judgment suggests that patients whose cardiac output and/or blood pressure depends on sympathetic stimulation are not good candidates for β-adrenergic blocker therapy for acute MI, and such use is not recommended for patients whose systolic blood pressure or heart rate persistently is less than 100 mm Hg or 50-60 beats/minute, respectively.

Since β-blockers may inhibit bronchodilation produced by endogenous catecholamines, the drugs generally should not be used in patients with bronchospastic disease; however, because of its relative β1-selective adrenergic blocking activity, atenolol may be used with caution in patients with bronchospastic disease who do not respond to or cannot tolerate other hypotensive agents. If atenolol is used in such patients, the initial dosage should be 50 mg daily and the smallest effective dosage should be used. In patients who develop symptoms of bronchospasm, atenolol dosage should be reduced or the drug discontinued (gradually if possible), and supportive treatment administered. In patients with bronchospastic disease, concomitant administration of a β2-adrenergic agonist and/or twice-daily dosing of the drug may minimize the risk of bronchospasm.

Abrupt withdrawal of atenolol may exacerbate angina symptoms and/or precipitate MI and ventricular arrhythmias in patients with coronary artery disease, or may precipitate thyroid storm in patients with thyrotoxicosis. Therefore, patients receiving atenolol (especially those with ischemic heart disease) should be warned not to interrupt or discontinue therapy without consulting their physician. Because coronary artery disease is common and may be undiagnosed, abrupt withdrawal also should be avoided in patients receiving atenolol for other conditions (e.g., hypertension). When atenolol is discontinued in patients with coronary artery disease or suspected thyrotoxicosis, the patients should be observed carefully; patients with coronary artery disease should be advised to temporarily limit their physical activity. If exacerbation of angina occurs or acute coronary insufficiency develops after atenolol therapy is interrupted or discontinued, treatment with the drug should be reinstituted, at least temporarily.

Patients who have a history of anaphylactic reactions to a variety of allergens reportedly may be more reactive to repeated accidental, diagnostic, or therapeutic challenges with such allergens while taking β-blockers. These patients may be unresponsive to usual doses of epinephrine or may develop a paradoxical response to epinephrine when used to treat anaphylactic reactions.

Atenolol should be used with caution in patients undergoing major surgery involving general anesthesia. The necessity of withdrawing β-adrenergic blocking therapy prior to major surgery is controversial. Severe, protracted hypotension and difficulty in restarting or maintaining a heart beat have occurred during surgery in some patients who have received β-blockers. As with other β-blockers, the effects of atenolol can be reversed by administration of β-agonists (e.g., dobutamine, isoproterenol). If atenolol is discontinued, this should be done 2 days before surgery. If patients continue to receive atenolol prior to or during surgery in which anesthetics with negative inotropic activity are used, the patients should be observed for signs and symptoms of heart failure; if vagal stimulation occurs, atropine may be administered.

Atenolol should be used with caution in patients with hyperthyroidism since the drug may mask the tachycardia associated with hyperthyroidism. In addition, it is recommended that atenolol be used with caution in patients with diabetes mellitus since β-blockers may mask the tachycardia associated with hypoglycemia (a few cases have been reported in patients with type 2 diabetes mellitus), and β-blockers, especially nonselective ones, may potentially precipitate severe, acute hyperglycemia. (See Cautions: Endocrine Effects.) However, many clinicians state that patients with diabetes mellitus may be particularly likely to experience a reduction in morbidity and mortality with the use of these drugs. β-Blockers usually will not mask dizziness and sweating seen with hypoglycemia.

Atenolol should be used with caution and in reduced dosage in patients with impaired renal function, especially when creatinine clearance is less than 35 mL/minute per 1.73 m. The manufacturers recommend that patients receiving atenolol after hemodialysis be administered the drug under close supervision in a hospital setting, since marked hypotension may occur.

Atenolol is contraindicated in patients with sinus bradycardia, AV block greater than first degree, cardiogenic shock, known hypersensitivity to any component of the drug formulations, and overt or decompensated cardiac failure. Atenolol-containing therapy is not recommended for use in patients with untreated pheochromocytoma.

Pediatric Precautions

Although safety and efficacy remain to be fully established in children, some experts have recommended pediatric dosages of atenolol for hypertension based on currently limited clinical experience.(See Hypertension: Monotherapy under Dosage and Administration.) For information on overall principles and expert recommendations for treatment of hypertension in pediatric patients, .

Geriatric Precautions

Clinical studies of atenolol (used for angina pectoris associated with coronary atherosclerosis or hypertension) and of atenolol in fixed combination with chlorthalidone (used for hypertension) did not include sufficient numbers of patients 65 years of age and older to determine whether geriatric patients respond differently than younger adults. In addition, in a large clinical study (ISIS-1) evaluating atenolol in 8037 patients for the management of suspected acute MI, 2644 patients (about 33%) were 65 years of age or older, and there were no overall differences in safety or efficacy observed between geriatric individuals and younger adults; however, geriatric patients with systolic blood pressure below 120 mmHg seemed less likely to benefit from atenolol therapy. Although other clinical experience has not revealed age-related differences in response to the drug, care should be taken in dosage selection of atenolol. Because of greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant disease and drug therapy in geriatric patients, the manufacturers suggest that patients in this age group receive initial dosages of the drug in the low end of the usual range.

The manufacturers state that evaluation of geriatric patients with hypertension or MI always should include assessment of renal function.

Mutagenicity and Carcinogenicity

No evidence of atenolol-induced mutagenicity was seen with an in vitro microbial test system (Ames test) with or without metabolic activation. Atenolol also was not mutagenic in in vivo cytogenicity tests in Chinese hamsters or the dominant lethal assay in mice.

No evidence of carcinogenicity was observed following administration of atenolol at dosages up to 300 mg/kg daily (up to 150 times the maximum recommended human antihypertensive dosage) for 18 months in mice or 18 or 24 months in rats. However, an increased incidence of benign adrenal medullary tumors in males and females, mammary fibroadenomas in females, and anterior pituitary adenomas and thyroid parafollicular cell carcinomas in males was observed at 24 months in rats receiving 500-1500 mg/kg of atenolol daily (250-750 times the maximum recommended human antihypertensive dosage).

Pregnancy, Fertility, and Lactation


Atenolol has been shown to cause a dose-related increase in embryonal and fetal resorptions in rats when given at dosages 25 or more times the maximum human antihypertensive dosage; similar effects were not observed in rabbits receiving atenolol dosages up to 12.5 times the maximum human antihypertensive dosage. Atenolol crosses the placenta and has been detected in cord blood. Atenolol can cause fetal harm when administered to pregnant women. There are no studies on use of the drug during the first trimester of pregnancy and the possibility of fetal injury cannot be excluded. Atenolol therapy initiated in the second trimester of pregnancy has been associated with birth of infants who were small for gestational age. Atenolol has been used effectively under close supervision for the management of hypertension during the third trimester in a limited number of women and was well tolerated, and apparently did not adversely affect the fetus. However, use of the drug for longer periods of time for the management of mild to moderate hypertension in pregnant women has been associated with intrauterine growth retardation. Neonates born to mothers who receive atenolol at parturition may be at risk for developing hypoglycemia and bradycardia. Caution is recommended when atenolol is administered during pregnancy. If atenolol is administered during pregnancy or if the patient becomes pregnant while receiving the drug, the patient should be informed of the potential hazard to the fetus.


Reproduction studies in male and female rats using atenolol dosages up to 200 mg/kg daily (100 times the maximum recommended human antihypertensive dosage) have not revealed evidence of impaired fertility.


Atenolol is distributed into milk. The drug distributes into milk in concentrations 1.5-6.8 times those in maternal serum. In at least one infant, potentially toxic serum atenolol concentrations (2 mcg/mL) have been reported 48 hours after discontinuance of breast-feeding. Neonates of mothers who receive atenolol during breast-feeding may be at risk of developing hypoglycemia and adverse β-adrenergic effects (e.g., bradycardia). Therefore, the manufacturers state that atenolol should be used cautiously in nursing women. Because clearance of the drug may be substantially impaired, premature neonates, and infants with impaired renal function, may be at increased risk of developing adverse effects from ingested atenolol during breast-feeding. If a woman receiving atenolol breast-feeds, the infant should be monitored closely for potential systemic effects of the drug. Alternatively, β-blockers that distribute less extensively into milk (e.g., propranolol) can be considered, although caution still must be exercised.

Drug Interactions

Cardiovascular Drugs

Concomitant administration of atenolol with reserpine may increase the incidence of hypotension and bradycardia as compared with atenolol alone, because of reserpine's catecholamine-depleting activity. Atenolol also is additive with and may potentiate the hypotensive actions of other hypotensive agents (e.g., calcium-channel blockers, hydralazine, methyldopa). This effect usually is used to therapeutic advantage, but dosage should be carefully adjusted when these drugs are used concurrently. Because β-blockers may exacerbate rebound hypertension that may occur following discontinuance of clonidine therapy, atenolol should be discontinued several days before clonidine when clonidine therapy is to be discontinued in patients receiving atenolol and clonidine concurrently.

Patients currently receiving another β-blocker must be evaluated carefully prior to initiating atenolol therapy. Depending on clinical findings (e.g., blood pressure, pulse), initial and subsequent atenolol dosage can be adjusted downward.

Slowing or complete suppression of SA node activity with development of slow ventricular rates (e.g., 30-40 bpm), often misdiagnosed as complete AV block, has been reported in patients receiving the nondihydropyridine calcium-channel blocking agent mibefradil (no longer commercially available in the US), principally in geriatric patients and in association with concomitant β-adrenergic blocker therapy.

Parenteral atenolol should be used with caution in patients who recently have received another drug that also may have a negative inotropic effect on the myocardium. Concomitant therapy with a β-blocker and verapamil can result in potentially serious adverse reactions, particularly in patients with severe cardiomyopathy, heart failure, or recent myocardial infarction (MI).

Nonsteroidal Anti-inflammatory Agents

Concurrent use of cyclooxygenase (prostaglandin synthase) inhibitors (e.g., indomethacin) may decrease the hypotensive effects of β-blockers. However, information on concomitant use of atenolol and aspirin is limited. Evidence from several studies (e.g., Thrombolysis in Myocardial Infarction Phase II [TIMI-II], Second International Study of Infarct Survival [ISIS-2]) suggests a lack of any clinically important adverse interaction and that the drugs can be used safely and effectively together in patients with MI.



Atenolol is rapidly but incompletely absorbed from the GI tract. Only about 50-60% of an oral dose of atenolol is absorbed. In healthy adults, peak plasma concentrations of 1-2 mcg/mL are achieved 2-4 hours after oral administration of a single 200-mg dose of atenolol. An approximately fourfold interindividual variation in plasma concentrations attained has been reported with a specific oral dose of atenolol. In geriatric patients, plasma concentrations are increased. Peak plasma atenolol concentrations are achieved within 5 minutes following direct IV injection of the drug, and decline rapidly during an initial distribution phase; after the first 7 hours, plasma concentrations reportedly decline with an elimination half-life similar to that of orally administered drug.

The effect of atenolol on heart rate usually has an onset of 1 hour, peaks at 2-4 hours, and persists for 24 hours following oral administration of the drug. Following IV administration of a single 10-mg dose, the effect on heart rate usually peaks within 5 minutes and generally is negligible by 12 hours after the dose. The antihypertensive and β-adrenergic blocking effect of a single 50- to 100-mg oral dose usually persists for 24 hours. Atenolol's effect on heart rate, but not on blood pressure, correlates linearly with plasma atenolol concentrations of 0.02-200 mcg/mL.


In animals, atenolol is well distributed into most tissues and fluids except brain and CSF. Unlike propranolol, only a small portion of atenolol is apparently distributed into the CNS.

Approximately 6-16% of atenolol is bound to plasma protein.

Atenolol readily crosses the placenta and has been detected in cord blood. During continuous administration, fetal serum concentrations of the drug are probably equivalent to those in maternal serum. Atenolol is distributed into milk; peak milk concentrations of the drug are higher than peak serum concentrations after an individual dose, and the area under the milk concentration-time curve (AUC) is substantially greater than that of the serum AUC in lactating women receiving the drug continuously.(See Cautions: Pregnancy, Fertility, and Lactation.)


In patients with normal renal function, atenolol has a plasma half-life(t½) of 6-7 hours. Children with normal renal function may exhibit a shorter elimination half-life. In one study in children 5-16 (mean: 8.9) years of age with arrhythmias and normal renal and hepatic function, the terminal elimination half-life averaged 4.6 hours. The plasma half-life(t½) of atenolol is markedly prolonged in geriatric patients compared with that in younger patients. Plasma t½ of the drug increases to 16-27 hours in patients with creatinine clearances of 15-35 mL/minute per 1.73 m and exceeds 27 hours with progressive renal impairment. Little or no metabolism of atenolol occurs in the liver. Approximately 40-50% of an oral dose of the drug is excreted in urine unchanged. The remainder is excreted unchanged in feces, principally as unabsorbed drug. About 1-12% of atenolol is reportedly removed by hemodialysis.

In geriatric patients, total plasma clearance of atenolol is reduced by about 50% compared with that in younger patients, resulting in higher plasma concentrations of the drug. The decreased clearance in geriatric adults may be related to decreased renal function in this age group.

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