Advise patients with coronary artery disease who are being treated with atenolol against abrupt discontinuation of therapy. Severe exacerbation of angina and the occurrence of myocardial infarction (MI) and ventricular arrhythmias have been reported in patients with angina following the abrupt discontinuation of therapy with beta-blockers. The last 2 complications may occur with or without preceding exacerbation of the angina pectoris. As with other beta-blockers, when discontinuation of atenolol is planned, observe the patient carefully and advise the patient to limit physical activity to a minimum. If the angina worsens or acute coronary insufficiency develops, it is recommended that atenolol be promptly reinstituted, at least temporarily. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue atenolol therapy abruptly, even in patients treated only for hypertension.
Dosage guidance:
Dosing: Dosage should be individualized based on patient response.
Hypertension: Children and Adolescents: Oral: Initial: 0.5 to 1 mg/kg/day either once daily or divided in doses twice daily; titrate dose to effect; maximum daily dose: 2 mg/kg/day not to exceed 100 mg/day (Ref).
Marfan syndrome, aortic-root dilation: Limited data available: Infants ≥6 months, Children, and Adolescents: Initial: 0.5 mg/kg/day; titrate based on tolerability and clinical goal (eg, heart rate); maximum daily dose: 4 mg/kg/day not to exceed 250 mg/day (Ref). Dosing interval not clearly defined in the literature; once daily or divided doses twice daily are the most common dosing intervals reported in the literature for other indications; may consider dividing doses twice daily in patients <10 years of age due to shorter elimination half-life (Ref). Dosing based on a randomized clinical trial (atenolol group: n=303, mean age 11.5 ± 6.5 years) comparing aortic root growth in patients with Marfan syndrome and baseline aortic-root z score >3, receiving atenolol or losartan; no significant difference in aortic-root dilation over a 3-year period was found between the two groups (Ref).
Tachycardia, supraventricular: Limited data available: Infants, Children, and Adolescents: Oral: Usual dose: 0.3 to 1 mg/kg/day either once daily or in divided doses every 12 hours; maximum daily dose: 2 mg/kg/day not to exceed 100 mg/day (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Altered kidney function: Infants, Children, and Adolescents: Oral:
GFR >50 mL/minute/1.73 m2: No dosage adjustment necessary (Ref).
GFR 30 to 50 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 24 hours; maximum adult daily dose: 50 mg/day (Ref).
GFR 10 to <30 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 48 hours (Ref); based on adult information, maximum dose should not exceed 50 mg/dose (Ref).
GFR <10 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 48 hours (Ref); based on adult information, maximum dose should not exceed 25 mg/dose (Ref).
Intermittent hemodialysis: Infants, Children, and Adolescents: Oral: Moderately dialyzable (20% to 50%) (Ref): Maximum dose: 1 mg/kg/dose every 48 hours; give after hemodialysis (Ref). Note: Usual adult dose is 25 to 50 mg/day (Ref).
Peritoneal dialysis: Infants, Children, and Adolescents: Oral: Not significantly dialyzed (Ref): Maximum dose: 1 mg/kg/dose every 48 hours (Ref); based on adult information, maximum dose should not exceed 25 mg/dose (Ref).
There are no dosage adjustments provided in the manufacturer's labeling; of note, atenolol undergoes limited hepatic metabolism.
(For additional information see "Atenolol: Drug information")
Angina, chronic stable:
Note: For vasospastic angina, beta-blockers are not recommended; calcium channel blockers and nitrates are preferred. For nonvasospastic angina, titrate beta-blocker to relieve angina or equivalent symptoms (Ref).
Oral: Initial: 50 mg once daily; may increase dose at weekly intervals based on frequency and severity of anginal symptoms and tolerability; usual dosage range: 50 to 100 mg once daily.
Atrial fibrillation/flutter, maintenance of ventricular rate control (off-label use):
Oral: Initial: 25 mg once daily; increase dose gradually as tolerated to achieve ventricular rate control up to 100 mg once daily (Ref).
Hypertension (alternative agent):
Note: Recommended only in patients with specific comorbidities (eg, myocardial infarction [MI], arrhythmia) (Ref).
Oral: Initial: 25 mg once or twice daily; titrate at ≥1 week intervals as needed based on response and tolerability up to 100 mg/day in 1 or 2 divided doses (Ref).
Marfan syndrome with aortic aneurysm (off-label use):
Note : Data for specific dosing are limited but a beta-blocker is recommended to slow aortic dilation (Ref).
Oral: Initial: 0.5 mg/kg once daily; titrate to maintain heart rate <100 beats per minute after submaximal exercise (eg, running up and down 2 flights of stairs); doses should be rounded to the nearest 25 mg increment; usual dosage range: 25 to 100 mg/day; maximum dose: 200 mg/day (Ref).
Migraine, prevention (alternative agent) (off-label use):
Note: An adequate trial for assessment of effect is considered to be at least 2 to 3 months at a therapeutic dose (Ref).
Oral: Initial: 25 mg once daily; titrate gradually (eg, every 1 to 2 weeks) based on response and tolerability up to 100 mg once daily (Ref).
Myocardial infarction, early treatment and secondary prevention:
Note: An oral beta-blocker is recommended within the first 24 hours for most patients. Patients who did not receive a beta-blocker within 24 hours of MI should be reevaluated for secondary prevention at a later date (Ref).
Oral: Initial: 25 to 50 mg twice daily; some experts suggest a starting dose of 12.5 mg once daily when there is concern for adverse effects; titrate as tolerated based on heart rate and BP up to a usual maximum dose of 100 mg/day administered in 1 or 2 divided doses (Ref). Optimal duration of therapy is unknown; reassess need for long-term beta-blocker use (>1 year) if no other primary indication exists (eg, angina, arrhythmia, hypertension) (Ref).
Supraventricular tachycardia (eg, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia, multifactorial atrial tachycardia), maintenance of ventricular rate control (off-label use):
Oral: Initial: 25 to 50 mg once daily; titrate based on response and tolerability; maximum recommended dose: 100 mg once daily (Ref).
Thyrotoxicosis (off-label use):
Note: For control of adrenergic symptoms until euthyroidism is established (Ref).
Oral: Initial: 25 to 50 mg once daily; titrate as needed to control symptoms (eg, tachycardia, palpitations, tremulousness) up to a maximum of 200 mg/day in 2 divided doses. Doses ≥50 mg/day can be administered in 2 divided doses if adrenergic symptoms become noticeable toward the end of the dosing interval with once daily dosing (Ref).
Ventricular arrhythmia or ventricular premature beats (symptomatic), prevention (off-label use):
Oral: Initial: 25 mg once daily; titrate dose as needed based on response and tolerability up to a maximum dose of 200 mg/day in 1 or 2 divided doses; usual dosage range: 25 to 100 mg/day (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function (Ref):
CrCl >30 mL/minute: No dosage adjustment necessary.
CrCl 10 to 30 mL/minute: Maximum dose: 50 mg daily.
CrCl <10 mL/minute: Maximum dose: 25 mg daily.
Hemodialysis, intermittent (thrice weekly): Moderately dialyzable (20% to 50%) (Ref):
Daily dosing: 25 to 50 mg daily; when scheduled dose falls on a dialysis day, administer post dialysis (Ref).
Three times weekly (post dialysis) dosing: Initial: 25 to 50 mg 3 times weekly administered post dialysis on dialysis days; titrate based on patient response to a maximum of 100 mg 3 times weekly administered post dialysis on dialysis days (Ref).
Peritoneal dialysis: Not significantly dialyzed (Ref): Maximum: 25 mg daily (Ref).
There are no dosage adjustments provided in the manufacturer’s labeling; however, atenolol undergoes minimal hepatic metabolism.
Beta-blockers may cause bradycardia or first, second, or third-degree atrioventricular (AV) heart block (Ref). At maintenance dosing, second- or third-degree AV block are less likely (Ref). Beta-blocking agents with intrinsic sympathomimetic activity (eg, pindolol) may cause fewer AV conduction abnormalities than those without intrinsic sympathomimetic activity (eg, atenolol) due to their partial agonist effects (Ref). In most cases (up to 72%), AV block associated with a beta-blocker will resolve upon discontinuation; however, there are reported cases of recurrent AV block and nearly 50% of patients with more severe AV block may require a permanent pacemaker (Ref).
Mechanism: Dose-related; related to the pharmacologic action. Blockade of cardiac beta-1 adrenergic receptors results in slowed conduction and prolongation in the refractory period of the AV node. Slowing of AV conduction can lead to AV block (Ref).
Onset: Varied; one study included patients who were on beta-blocker for more than 1 month (Ref); however, other studies noted prolongation of the PR interval or AV nodal refractory period occurring anywhere from 1 dose to several days following treatment initiation (Ref).
Risk factors:
• Impaired AV node or sinus node conduction (Ref)
• Concurrent use of other agents that impair AV nodal conduction (eg, nondihydropyridine calcium channel blockers, digoxin, ivabradine, select antiarrhythmic agents) (Ref)
• Older patients (Ref)
• Hyperkalemia (Ref)
• Kidney impairment, including dialysis dependence (Ref)
Selective beta-blockers (eg, atenolol) have a lower risk of bronchospasm compared to non-cardioselective beta-blockers (Ref). While atenolol is associated with worsening bronchoconstriction and FEV1, there appears to be no change in overall day-to-day asthma control with use (Ref). Of the beta-blockers, atenolol has been associated with the least incidence of asthma attacks (Ref). Concurrent use of inhaled bronchodilators and/or corticosteroids are protective against beta-blocker–induced bronchospasm in patients with chronic obstructive pulmonary disease or asthma (Ref). Bronchospasm is reversible upon discontinuation or use of bronchodilators (Ref).
Mechanism: Dose-related; related to pharmacologic action. Beta-blocking agents can lead to airway smooth muscle constriction by antagonism of beta-2 receptors (Ref).
Onset: Rapid (Ref).
Risk factors:
• Acute use (reports suggest that single doses or acute use are more likely to cause changes in FEV1 compared to chronic use) (Ref)
Beta-blockers may cause reversible CNS effects such as fatigue, insomnia, vivid dreams, memory impairment, and sexual disorder (Ref). Sexual disorders may occur; however, patients who require beta-blocker therapy may have risk factors for erectile dysfunction (eg, coronary artery disease, heart failure) (Ref). In addition, there may be a psychosomatic component (Ref). Hydrophilic beta-blockers, such as atenolol, penetrate the blood-brain barrier to a lesser extent than lipophilic beta-blockers, possibly leading to a lower incidence of CNS effects; however, other studies have refuted this theory (Ref). CNS effects generally resolve with dose reduction or discontinuation (Ref).
Mechanism: Dose-related; exact mechanism is not fully understood. Proposed mechanisms include presence of beta receptors in the brain, affinity, and in some instances, inhibition of beta-blocking agents towards serotonin (5-HT) receptors in the brain (affecting mood and sleep), and beta-blocker–induced decreases in central sympathetic output (Ref). Beta-1 blockade may also impact sleep by blocking sympathetic signaling to the pineal gland, resulting in suppression of nighttime levels of melatonin (Ref). Beta-blockers may cause erectile dysfunction through decreased sympathetic nervous system output and subsequent decreases in luteinizing hormone secretion and testosterone stimulation (Ref).
Onset: Intermediate; CNS effects often occur within the first few weeks of treatment (Ref).
Risk factors:
• Older patients (Ref)
• Higher starting doses (Ref)
Beta-blockers may worsen, prolong, or cause hypoglycemia (Ref). Additionally, beta-blockers may mask symptoms of hypoglycemia (tremor, irritability, palpitations), making diaphoresis the only symptom unaffected by beta-blockers (Ref). It is unclear if nonselective or selective beta-blockers are more likely to cause hypoglycemia as data are conflicting (Ref).
Mechanism: Dose-related; related to the pharmacologic action. Beta-blockers inhibit hepatic gluconeogenesis and glycogenolysis (Ref). Beta-blockers also reduce activation of the sympathetic nervous system, therefore masking hypoglycemic symptoms that are catecholamine-mediated (Ref).
Onset: Varied; data are limited for atenolol; onset is extrapolated from other beta blocking agents: Blood glucose recovery was significantly reduced following 1 dose or 1 day of therapy (Ref); in another study, episodes of severe hypoglycemia were reported over the course of 4 years (Ref).
Risk factors:
• Insulin-dependent diabetes (Ref)
• Type 2 diabetes mellitus (Ref)
• Hospitalized patients not requiring basal insulin (Ref)
Beta-blocker therapy should not be withdrawn abruptly, but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia in patients with underlying cardiovascular disease (Ref). Some studies have found an increase in propensity-adjusted mortality and cardiovascular events; however, one study did not find changes in infarct size and left ventricular function when beta-blocker was abruptly withdrawn in patients with myocardial infarction (Ref). Additionally, another study assessing effects of abrupt withdrawal of atenolol in patients with severe angina did not show any catastrophic coronary events (Ref).
Mechanism: Dose dependent; related to the pharmacologic action. Beta blockade causes upregulation of beta-receptors, enhanced receptor sensitivity, and decreased sympathetic nervous system response (Ref). Abrupt withdrawal leads to a transient sympathetic hyper-response (Ref). Another proposed mechanism involves increased platelet aggregability to epinephrine and thrombin (Ref).
Onset: Rapid/varied and transient; increases in heart rate and blood pressure appear 24 hours after abrupt withdrawal, peak after 48 hours, and subside after 7 days (Ref).
Risk factors:
• Abrupt withdrawal in chronic users (Ref)
• Past medical history of coronary artery disease (including chronic stable angina) (Ref)
• Past medical history of hypertension (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Incidence rates are from studies in hypertensive patients unless otherwise noted.
>10%:
Cardiovascular: Bradycardia (3%; in patients with acute myocardial infarction: 18%) (table 1) , heart failure (in patients with acute myocardial infarction: 19%) (table 2) , hypotension (in patients with acute myocardial infarction: 25%), supraventricular tachycardia (in patients with acute myocardial infarction: 12%), ventricular tachycardia (in patients with acute myocardial infarction: 16%)
Drug (Atenolol) |
Conventional Therapy |
Placebo |
Indication |
Number of Patients (Atenolol) |
Number of Patients (Conventional Therapy) |
Number of Patients (Placebo) |
Comments |
---|---|---|---|---|---|---|---|
18% |
10% |
N/A |
Acute myocardial infarction |
244 |
233 |
N/A |
Conventional therapy plus atenolol |
3% |
N/A |
0% |
Hypertension |
164 |
N/A |
206 |
N/A |
Drug (Atenolol) |
Conventional Therapy |
Placebo |
Indication |
Number of Patients (Atenolol) |
Number of Patients (Conventional Therapy) |
Number of Patients (Placebo) |
Comments |
---|---|---|---|---|---|---|---|
19% |
24% |
N/A |
Acute myocardial infarction |
244 |
233 |
N/A |
Conventional therapy plus atenolol |
1% to 10%:
Cardiovascular: Atrial fibrillation (in patients with acute myocardial infarction: 5%), atrial flutter (in patients with acute myocardial infarction: 2%), bundle branch block (in patients with acute myocardial infarction: 7%), heart block (in patients with acute myocardial infarction: 5%) (table 3) , orthostatic hypotension (2%), pulmonary embolism (in patients with acute myocardial infarction: 1%)
Drug (Atenolol) |
Conventional Therapy |
Placebo |
Indication |
Number of Patients (Atenolol) |
Number of Patients (Conventional Therapy) |
Number of Patients (Placebo) |
Comments |
---|---|---|---|---|---|---|---|
5% |
4% |
N/A |
Acute myocardial infarction |
244 |
233 |
N/A |
Conventional therapy plus atenolol |
Gastrointestinal: Diarrhea (2%), nausea (4%)
Nervous system: Dizziness (1% to 4%), fatigue (≤3%) (table 4) , lethargy (1%), vertigo (2%)
Drug (Atenolol) |
Conventional Therapy |
Placebo |
Indication |
Number of Patients (Atenolol) |
Number of Patients (Conventional Therapy) |
Number of Patients (Placebo) |
Comments |
---|---|---|---|---|---|---|---|
3% |
N/A |
1% |
Hypertension |
164 |
N/A |
206 |
N/A |
0.6% |
N/A |
0.5% |
Hypertension |
164 |
N/A |
206 |
Described as "tiredness" |
Respiratory: Bronchospasm (in patients with acute myocardial infarction: 1%) (table 5)
Drug (Atenolol) |
Conventional Therapy |
Placebo |
Indication |
Number of Patients (Atenolol) |
Number of Patients (Conventional Therapy) |
Number of Patients (Placebo) |
Comments |
---|---|---|---|---|---|---|---|
1% |
0.9% |
N/A |
Acute myocardial infarction |
244 |
233 |
N/A |
Conventional therapy plus atenolol |
<1%:
Cardiovascular: Cardiogenic shock
Nervous system: Drowsiness
Renal: Renal failure syndrome
Frequency not defined:
Cardiovascular: Raynaud disease (Marshall 1976)
Immunologic: Antibody development
Neuromuscular & skeletal: Lupus-like syndrome (Gouet 1986)
Postmarketing:
Cardiovascular: Sick sinus syndrome (Neto 2022)
Dermatologic: Exacerbation of psoriasis (Yilmaz 2022), psoriasiform eruption (Wakefield 1990), transient alopecia
Gastrointestinal: Xerostomia
Genitourinary: Impotence, Peyronie disease
Hematologic & oncologic: Purpuric disease, thrombocytopenia
Hepatic: Increased liver enzymes, increased serum bilirubin
Nervous system: Hallucination, headache, psychosis (Viadero 1983)
Ophthalmic: Visual disturbance
Hypersensitivity to atenolol or any component of the formulation; sinus bradycardia; heart block greater than first-degree (except in patients with a functioning artificial pacemaker); cardiogenic shock; uncompensated cardiac failure
Canadian labeling: Additional contraindications (not in US labeling): Bradycardia (regardless of origin); cor pulmonale; hypotension; severe peripheral arterial disorders; anesthesia with agents that produce myocardial depression; Pheochromocytoma (in the absence of alpha-blockade); metabolic acidosis
Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Disease-related concerns:
• Anaphylaxis: Beta-blockers are unlikely to cause anaphylaxis; however, in susceptible patients, beta-blockers have been associated with an increase in the severity of anaphylaxis. Anaphylaxis in the presence of a beta-blocker may be severe, protracted, and resistant to conventional treatment (Lang 2008; Toogood 1987).
• Heart failure: Stabilize patients on heart failure regimen prior to initiation or titration of beta-blocker. Beta-blocker therapy should be initiated at very low doses with gradual and very careful titration. Adjustment of other medications (angiotensin-converting enzyme inhibitors and/or diuretics) may be required. Efficacy of atenolol in heart failure has not been demonstrated as with other beta-blockers.
• Myasthenia gravis: Use with caution in patients with myasthenia gravis.
• Peripheral vascular disease (PVD) and Raynaud disease: May precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud disease. Use with caution and monitor for progression of arterial obstruction.
• Pheochromocytoma (untreated): Adequate alpha-blockade is required prior to use of any beta-blocker.
• Psoriasis: Beta-blocker use has been associated with induction or exacerbation of psoriasis, but cause and effect have not been firmly established.
• Renal impairment: Use with caution in patients with renal impairment; dosage adjustment required.
• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If hyperthyroidism is suspected, carefully manage and monitor; abrupt withdrawal may precipitate thyroid storm. Alterations in thyroid function tests may be observed.
• Vasospastic angina: Beta-blockers without alpha1-adrenergic receptor blocking activity should be avoided in patients with Prinzmetal variant angina since unopposed alpha1-adrenergic receptors mediate coronary vasoconstriction and can worsen anginal symptoms (Mayer 1998).
Other warnings/precautions:
• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Tenormin: 25 mg, 50 mg
Tenormin: 50 mg [scored]
Tenormin: 100 mg
Generic: 25 mg, 50 mg, 100 mg
Yes
Tablets (Atenolol Oral)
25 mg (per each): $0.24 - $0.82
50 mg (per each): $0.79 - $0.83
100 mg (per each): $1.22 - $1.49
Tablets (Tenormin Oral)
25 mg (per each): $16.03
50 mg (per each): $16.03
100 mg (per each): $16.03
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Tenormin: 50 mg, 100 mg [contains corn starch]
Generic: 25 mg, 50 mg, 100 mg
2 mg/mL Oral Suspension (ASHP Standard Concentration) (ASHP 2017)
A 2 mg/mL oral suspension may be made with tablets. Crush four 50 mg tablets in a mortar and reduce to a fine powder. Add a small amount of glycerin and mix to a uniform paste. Mix while adding Ora-Sweet SF vehicle in incremental proportions to almost 100 mL; transfer to a calibrated amber bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 100 mL. Label “shake well”. Stable for 90 days at room temperature.
Oral: May be administered without regard to food
Oral: May be administered without regard to meals.
Store at 20°C to 25°C (68°F to 77°F).
Treatment of hypertension, alone or in combination with other agents (FDA approved in adults); long-term management of angina pectoris (FDA approved in adults); management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality (FDA approved in adults); has also been used for management of supraventricular tachycardia, infantile hemangioma, Marfan syndrome (prevention of aortic-root dilation), and thyrotoxicosis.
Atenolol may be confused with albuterol, Altenol, timolol, Tylenol
Tenormin may be confused with Imuran, Norpramin, thiamine, Trovan
Substrate of OCT1, OCT2;
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program
Acetylcholinesterase Inhibitors: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Alfuzosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Alpha2-Agonists: Beta-Blockers may increase rebound hypertensive effects of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Alpha2-Agonists may increase AV-blocking effects of Beta-Blockers. Sinus node dysfunction may also be enhanced. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider Therapy Modification
Amifostine: Blood Pressure Lowering Agents may increase hypotensive effects of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider Therapy Modification
Amiodarone: May increase bradycardic effects of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase serum concentration of Beta-Blockers. Risk C: Monitor
Amphetamines: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor
Ampicillin: May decrease bioavailability of Atenolol. Risk C: Monitor
Antidiabetic Agents: Beta-Blockers (Beta1 Selective) may increase adverse/toxic effects of Antidiabetic Agents. Specifically, beta-blockers may mask the hypoglycemic symptoms of antidiabetic agents. Risk C: Monitor
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may increase hypotensive effects of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor
Arginine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Bacampicillin: May decrease bioavailability of Atenolol. Risk C: Monitor
Barbiturates: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Benperidol: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Beta2-Agonists: Beta-Blockers (Beta1 Selective) may decrease bronchodilatory effects of Beta2-Agonists. Of particular concern with nonselective beta-blockers or higher doses of the beta1 selective beta-blockers. Risk C: Monitor
Bradycardia-Causing Agents: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Brigatinib: May decrease antihypertensive effects of Antihypertensive Agents. Brigatinib may increase bradycardic effects of Antihypertensive Agents. Risk C: Monitor
Brimonidine (Topical): May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Bromperidol: May decrease hypotensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase hypotensive effects of Bromperidol. Risk X: Avoid
Cafedrine: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Cafedrine. Risk C: Monitor
Cannabis: Beta-Blockers may increase adverse/toxic effects of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor
Ceritinib: Bradycardia-Causing Agents may increase bradycardic effects of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider Therapy Modification
Cholinergic Agonists: Beta-Blockers may increase adverse/toxic effects of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor
Dexmethylphenidate: May decrease therapeutic effects of Antihypertensive Agents. Risk C: Monitor
Diazoxide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Dipyridamole: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Disopyramide: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may increase negative inotropic effects of Disopyramide. Risk C: Monitor
DOBUTamine: Beta-Blockers may decrease therapeutic effects of DOBUTamine. Risk C: Monitor
Dronedarone: May increase bradycardic effects of Beta-Blockers. Dronedarone may increase serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Increase monitoring for clinical response and adverse effects. Risk D: Consider Therapy Modification
DULoxetine: Blood Pressure Lowering Agents may increase hypotensive effects of DULoxetine. Risk C: Monitor
EPHEDrine (Systemic): Beta-Blockers may decrease therapeutic effects of EPHEDrine (Systemic). Risk C: Monitor
EPINEPHrine (Nasal): Beta-Blockers (Beta1 Selective) may decrease therapeutic effects of EPINEPHrine (Nasal). Risk C: Monitor
EPINEPHrine (Oral Inhalation): Beta-Blockers (Beta1 Selective) may decrease therapeutic effects of EPINEPHrine (Oral Inhalation). Risk C: Monitor
EPINEPHrine (Systemic): Beta-Blockers (Beta1 Selective) may decrease therapeutic effects of EPINEPHrine (Systemic). Risk C: Monitor
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may increase vasoconstricting effects of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor
Etilefrine: Beta-Blockers may decrease therapeutic effects of Etilefrine. Etilefrine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Etofylline: Beta-Blockers may decrease therapeutic effects of Etofylline. Risk X: Avoid
Etrasimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Fexinidazole: Bradycardia-Causing Agents may increase arrhythmogenic effects of Fexinidazole. Risk X: Avoid
Fingolimod: Bradycardia-Causing Agents may increase bradycardic effects of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider Therapy Modification
Flunarizine: May increase therapeutic effects of Antihypertensive Agents. Risk C: Monitor
Glycopyrrolate (Systemic): May increase serum concentration of Atenolol. Risk C: Monitor
Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may increase adverse/toxic effects of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider Therapy Modification
Herbal Products with Blood Pressure Increasing Effects: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor
Herbal Products with Blood Pressure Lowering Effects: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Hypotension-Associated Agents: Blood Pressure Lowering Agents may increase hypotensive effects of Hypotension-Associated Agents. Risk C: Monitor
Iloperidone: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Indoramin: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor
Isocarboxazid: May increase antihypertensive effects of Antihypertensive Agents. Risk X: Avoid
Isoproterenol: Beta-Blockers may decrease therapeutic effects of Isoproterenol. Risk C: Monitor
Ivabradine: Bradycardia-Causing Agents may increase bradycardic effects of Ivabradine. Risk C: Monitor
Lacosamide: Bradycardia-Causing Agents may increase AV-blocking effects of Lacosamide. Risk C: Monitor
Landiolol: Bradycardia-Causing Agents may increase bradycardic effects of Landiolol. Risk X: Avoid
Levodopa-Foslevodopa: Blood Pressure Lowering Agents may increase hypotensive effects of Levodopa-Foslevodopa. Risk C: Monitor
Loop Diuretics: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor
Lormetazepam: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Mavacamten: Beta-Blockers may increase adverse/toxic effects of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor
Metergoline: May decrease antihypertensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase orthostatic hypotensive effects of Metergoline. Risk C: Monitor
Methacholine: Beta-Blockers may increase adverse/toxic effects of Methacholine. Risk C: Monitor
Methylphenidate: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor
Midodrine: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Mivacurium: Beta-Blockers may increase therapeutic effects of Mivacurium. Risk C: Monitor
Molsidomine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Naftopidil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Nicergoline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Nicorandil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
NIFEdipine (Topical): May increase adverse/toxic effects of Beta-Blockers. Risk C: Monitor
NIFEdipine: May increase hypotensive effects of Beta-Blockers. NIFEdipine may increase negative inotropic effects of Beta-Blockers. Risk C: Monitor
Nitrendipine: May increase therapeutic effects of Beta-Blockers. Risk C: Monitor
Nitroprusside: Blood Pressure Lowering Agents may increase hypotensive effects of Nitroprusside. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents (Topical): May decrease therapeutic effects of Beta-Blockers. Risk C: Monitor
Nonsteroidal Anti-Inflammatory Agents: May decrease antihypertensive effects of Beta-Blockers. Risk C: Monitor
Obinutuzumab: May increase hypotensive effects of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider Therapy Modification
Opipramol: Beta-Blockers may increase serum concentration of Opipramol. Opipramol may increase serum concentration of Beta-Blockers. Risk C: Monitor
Ozanimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor
Pentoxifylline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Perazine: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor
Pholcodine: Blood Pressure Lowering Agents may increase hypotensive effects of Pholcodine. Risk C: Monitor
Phosphodiesterase 5 Inhibitors: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Ponesimod: Bradycardia-Causing Agents may increase bradycardic effects of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider Therapy Modification
Prazosin: Antihypertensive Agents may increase hypotensive effects of Prazosin. Risk C: Monitor
Prostacyclin Analogues: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Quinagolide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Reserpine: May increase hypotensive effects of Beta-Blockers. Reserpine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor
Rivastigmine: May increase bradycardic effects of Beta-Blockers. Risk X: Avoid
Silodosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor
Siponimod: Bradycardia-Causing Agents may increase bradycardic effects of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider Therapy Modification
Succinylcholine: Beta-Blockers may increase neuromuscular-blocking effects of Succinylcholine. Risk C: Monitor
Tasimelteon: Beta-Blockers may decrease therapeutic effects of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider Therapy Modification
Terazosin: Antihypertensive Agents may increase hypotensive effects of Terazosin. Risk C: Monitor
Theodrenaline: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Theodrenaline. Risk C: Monitor
Theophylline Derivatives: Beta-Blockers (Beta1 Selective) may decrease bronchodilatory effects of Theophylline Derivatives. Risk C: Monitor
Urapidil: Antihypertensive Agents may increase hypotensive effects of Urapidil. Risk C: Monitor
White Birch Allergen Extract: Beta-Blockers may increase adverse/toxic effects of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid
Atenolol serum concentrations may be decreased if taken with food. Management: Administer without regard to meals.
Medications considered acceptable for the treatment of chronic hypertension during pregnancy may generally be used in patients trying to conceive. Atenolol is not considered a preferred agent for use in pregnant patients; consider transitioning to a preferred agent in patients planning to become pregnant (ACC/AHA [Whelton 2018]; ACOG 2019).
Atenolol is effective for prevention of migraines. In general, preventive treatment for migraine in patients trying to become pregnant should be avoided. Options for patients planning a pregnancy should be considered as part of a shared decision-making process. Nonpharmacologic interventions should be considered initially. When needed, preventive treatment should be individualized considering the available safety data and needs of the patient should pregnancy occur. A gradual discontinuation of preventive medications is generally preferred when the decision is made to stop treatment prior to conception (ACOG 2022; AHS [Ailani 2021]).
Impotence is noted in product labeling following postmarketing use of atenolol. As a class, outcomes from available studies evaluating beta-blockers and sexual dysfunction are inconsistent, and the negative effects on erectile function and libido are considered controversial. A clear relationship between use of beta-blockers and erectile dysfunction has not been established. Hypertension itself is associated with erectile dysfunction. Patients on a beta-blocker presenting with sexual dysfunction should be evaluated for underlying disease (Farmakis 2021; Levine 2012; Semet 2017; Terentes-Printzios 2022; Viigimaa 2020).
Atenolol crosses the placenta and is found in cord blood.
Maternal use of atenolol may cause harm to the fetus. Adverse events, such as bradycardia, hypoglycemia and reduced birth weight, have been observed following in utero exposure to atenolol. If maternal use of a beta-blocker is needed, monitor fetal growth during pregnancy; monitor the newborn for 48 hours after delivery for bradycardia, hypoglycemia, and respiratory depression (ESC [Regitz-Zagrosek 2018]).
Chronic maternal hypertension is also associated with adverse events in the fetus/infant. Chronic maternal hypertension may increase the risk of birth defects, low birth weight, premature delivery, stillbirth, and neonatal death. Actual fetal/neonatal risks may be related to the duration and severity of maternal hypertension. Untreated chronic hypertension may also increase the risks of adverse maternal outcomes, including gestational diabetes, preeclampsia, delivery complications, stroke, and myocardial infarction (ACOG 2019).
The maternal pharmacokinetic parameters of atenolol during the second and third trimesters are within the ranges reported in nonpregnant patients (Hebert 2005).
When treatment of chronic hypertension during pregnancy is indicated, atenolol is not recommended due to adverse fetal/neonatal events (ACOG 2019; ESC [Cífková 2020]; ESC [Regitz-Zagrosek 2018]). Atenolol is also not recommended for the treatment of atrial fibrillation or supraventricular tachycardia during pregnancy; consult current guidelines for specific recommendations (ESC [Regitz-Zagrosek 2018]).
In general, preventive treatment for migraine should be avoided during pregnancy. Options for pregnant patients should be considered as part of a shared decision-making process. Nonpharmacologic interventions should be considered initially. When needed, preventive treatment should be individualized considering the available safety data, the potential for adverse maternal and fetal events, and needs of the patient (ACOG 2022; AHS [Ailani 2021]). If preventive therapy is needed, beta-blockers may be considered (ACOG 2022) however agents other than atenolol may be preferred (CHS [Pringsheim 2012]).
Blood pressure, heart rate, ECG, respiratory rate, and signs and symptoms of hypoglycemia with oral administration (especially in infants and young children).
Competitively blocks response to beta-adrenergic stimulation, selectively blocks beta1-receptors with little or no effect on beta2-receptors except at high doses
Onset of action: Beta-blocking effect: Onset: Oral: ≤1 hour; Peak effect: Oral: 2 to 4 hours
Duration: Normal renal function: Beta-blocking effect: 12 to 24 hours; Antihypertensive effect: Oral: 24 hours
Absorption: Oral: Rapid, incomplete (~50%)
Distribution: Low lipophilicity; does not cross blood-brain barrier
Protein binding: 6% to 16%
Metabolism: Limited hepatic
Half-life elimination: Beta:
Newborns (<24 hours of age) born to mothers receiving atenolol: Mean: 16 hours; up to 35 hours (Rubin 1983)
Children and Adolescents 5 to 16 years of age: Mean: 4.6 hours; range: 3.5 to 7 hours; Patients >10 years of age may have longer half-life (>5 hours) compared to children 5 to 10 years of age (<5 hours) (Buck 1989)
Adults: Normal renal function: 6 to 7 hours, prolonged with renal impairment; End-stage renal disease (ESRD): 15 to 35 hours
Time to peak, plasma: Oral: 2 to 4 hours
Excretion: Feces (50%); urine (40% as unchanged drug)
Altered kidney function: Elimination is closely related to glomerular filtration rate. Significant accumulation occurs when CrCl falls below 35 mL/minute per 1.73 m2.
Older adult: Total clearance is about 50% lower than in younger subjects. Half-life is markedly longer in older adults.