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Nadolol is used for the management of hypertension and angina. Nadolol has been used for the management of supraventricular tachyarrhythmias (e.g., atrial flutter or fibrillation) and for the prophylaxis of sinus 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, many clinicians prefer to use low dosages of a β1-selective adrenergic blocking agent (e.g., atenolol, metoprolol), rather than a nonselective agent like nadolol, in patients with chronic obstructive pulmonary disease (COPD) or insulin-dependent diabetes mellitus. However, selectivity of these agents is relative and dose dependent. Some clinicians also will recommend using a β1-selective agent or pindolol (because of its intrinsic sympathomimetic activity), 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.


Nadolol is used alone or in combination with other classes of antihypertensive agents in the management of hypertension. 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, myocardial infarction (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 (angiotensin-converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, or thiazide diuretics). and

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. Although β-blockers have lowered blood pressure in all races studied, monotherapy with these agents has produced a smaller reduction in blood pressure in black hypertensive patients; however, this population difference in response does not appear to occur during combined therapy with a β-blocker and a thiazide diuretic. and

In contrast to many other antihypertensive agents, nadolol and other β-blockers lower blood pressure equally well in the upright or supine position. The drug appears to be safe and effective in the treatment of hypertension in patients with renal damage. Nadolol reduces blood pressure in patients with low, normal, or elevated plasma renin levels. Tolerance to the hypotensive effect of nadolol apparently does not occur during long-term treatment.

For additional information on the role of β-blockers in the management of hypertension, and . For information on overall principles and expert recommendations for treatment of hypertension, .

Chronic Stable Angina

Nadolol is used for the long-term 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 use. Long-term use of β-blockers in patients with chronic stable angina has been shown to reduce the frequency of anginal attacks, allow a decrease 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.)

Supraventricular Tachyarrhythmias

Nadolol has been used in patients with atrial flutter or fibrillation for the management of frequent ventricular premature complexes, paroxysmal atrial tachycardia, and sinus tachycardia and to decrease heart rate.

Vascular Headaches


Nadolol has been used for the prophylaxis of migraine headache. The US Headache Consortium states that there is some evidence of efficacy for this indication from randomized clinical trials of the drug and that clinical experience suggests that nadolol produces clinically important improvement in most patients receiving the drug for migraine prophylaxis.

Dosage and Administration


Nadolol is administered orally once daily.


Since there is no consistent interpatient correlation between the dosage of nadolol and therapeutic response, dosage must be individualized according to the response of the patient. If long-term nadolol therapy is to be discontinued, dosage of the drug should be gradually reduced over a period of 1-2 weeks. (See Cautions: Precautions and Contraindications.)


Nadolol Therapy

For the management of hypertension, the initial adult dosage of nadolol is 20-40 mg daily, either alone or in combination with a diuretic. The manufacturers state that dosage may be gradually increased in increments of 40-80 mg daily until optimum blood pressure response is achieved. The usual adult maintenance dosage of nadolol recommended by the manufacturers is 40-80 mg daily, although dosages up to 240 or 320 mg daily may be needed. Some experts recommend a usual dosage range of 40-120 mg daily; the rationale for this reduced dosage range is that it usually is preferable to add another antihypertensive agent to the regimen than to continue increasing nadolol dosage since the patient may not tolerate such continued increases.

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. Target dosages of antihypertensive agents generally can be achieved within 2-4 weeks, but it may take up to several months.

In patients who experience intolerable adverse effects with nadolol, 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.

Nadolol/Bendroflumethiazide Combination Therapy

Although nadolol is available in fixed combination with bendroflumethiazide, preparations of bendroflumethiazide alone are no longer commercially available in the US. The manufacturer states that bendroflumethiazide alone usually was administered at a dosage of 5 mg daily, and the usual initial dosage of nadolol is 40 mg once daily, whether used alone or in combination with a diuretic. Therefore, the initial dosage of the fixed combination may be 40 mg of nadolol and 5 mg of bendroflumethiazide once daily. If needed, dosage may be increased to the fixed-combination preparation containing 80 mg of nadolol and 5 mg of bendroflumethiazide administered once daily. The manufacturer cautions that bendroflumethiazide in the fixed-combination preparation with nadolol is about 30% more bioavailable than the drug alone. If blood pressure is not adequately controlled with the fixed combination alone, another nondiuretic hypotensive agent can be added gradually, starting with 50% of the usual recommended starting dosage in order to avoid excessive reduction in blood pressure.

The manufacturers state that commercially available preparations containing nadolol in fixed combination with bendroflumethiazide should not be used for initial antihypertensive therapy.

Blood Pressure Monitoring and Treatment Goals

Careful monitoring of blood pressure during initial titration or subsequent upward adjustment in dosage of nadolol 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.

Chronic Stable Angina

For the management of angina pectoris, the initial adult dosage of nadolol is 40 mg daily. Dosage is gradually increased by 40-80 mg daily at 3- to 7-day intervals until optimum control of angina is obtained or there is pronounced slowing of the heart rate (i.e., to less than 55 beats/minute). The usual maintenance dosage of nadolol is 40 or 80 mg daily, but there is wide variation in individual requirements and dosage must be carefully titrated to achieve optimum results. Nadolol dosages up to 160 or 240 mg daily may be needed. The value and safety of dosage greater than 240 mg daily have not been established. During chronic therapy, the patient should be periodically reevaluated to determine the need for dosage alteration or continued therapy.

Supraventricular Tachyarrhythmias

In patients with various cardiac arrhythmias, maintenance nadolol dosages of 60-160 mg daily in single or divided doses have been used.

Vascular Headaches


The usual effective dosage for the prophylaxis of migraine headache is 80-240 mg daily.

Dosage in Renal Impairment

In patients with renal impairment, the usual dose of nadolol alone or in fixed combination with bendroflumethiazide is given at the following intervals depending on the patient's creatinine clearance:

Creatinine Clearance (mL/minute per 1.73 m2) Dosage Interval
>50 every 24 h
31-50 every 24-36 h
10-30 every 24-48 h
<10 every 40-60 h


Most adverse effects of nadolol are mild and transient and occur more frequently at the onset of therapy than during prolonged treatment. The most common, serious adverse effects of nadolol are related to its β-adrenergic blocking activity. Severe reactions result from the inability of severely ill patients to withstand a decrease in normal β-adrenergic stimulation.

Cardiovascular Effects

The most common adverse cardiovascular effects of nadolol are bradycardia (heart rate less than 60 beats/minute) and peripheral vascular insufficiency, usually of the Raynaud's type. Heart rates less than 40 beats/minute and/or symptomatic bradycardia, and peripheral vascular insufficiency have occurred in about 2% of patients. Severe bradycardia should be treated with IM or IV administration of atropine sulfate. If there is an inadequate response to atropine, IV isoproterenol may be administered with caution; large doses may be required. (See Drug Interactions: Sympathomimetic Agents.) Cardiac failure, postural hypotension, palpitation, and disturbances in cardiac rhythm and conduction have each occurred in about 1% of patients. In patients without a prior history of heart failure, prolonged depression of the myocardium by nadolol may result in heart failure in rare instances. First- and third-degree AV block have occurred and intensification of AV block which has occurred with other β-adrenergic blocking agents (β-blockers) may occur with nadolol.

During surgery, some patients who have received β-adrenergic blockers may experience severe, protracted hypotension, low cardiac output, or difficulty in restarting and maintaining heart beat. The untoward effects of nadolol may be reversed during surgery by IV administration of β-adrenergic agonists (e.g., isoproterenol, dopamine, or dobutamine).

CNS Effects

The most common adverse CNS effects of nadolol are dizziness and fatigue, which occur in about 2% of patients. Paresthesia, sedation, malaise, and change in behavior have occurred less frequently. Insomnia and sleep disturbances have been reported, but a causal relationship to nadolol has not been established. Potential adverse CNS effects include reversible mental depression progressing to catatonia, visual disturbances, hallucinations, an acute reversible syndrome characterized by disorientation to time and place, short-term memory loss, emotional lability with slightly clouded sensorium, and decreased performance on neuropsychometric tests.

GI Effects

GI symptoms such as nausea, diarrhea, abdominal discomfort, constipation, vomiting, indigestion, anorexia, bloating, and flatulence have occurred in about 0.1-0.5% of patients receiving nadolol.

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 type 2 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 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

Bronchospasm has occurred in about 0.1% of patients receiving nadolol. Other adverse effects which have occurred infrequently in patients receiving the drug include rash; pruritus; headache; dry mouth, eyes, and skin; reversible alopecia; impotence or decreased libido; facial swelling; weight gain; slurred speech; cough; nasal stuffiness; sweating; tinnitus; blurred vision; weakness; and numbness.

Potential hematologic effects of β-blockers include agranulocytosis and thrombocytopenic or nonthrombocytopenic purpura. Potential adverse allergic effects include fever with aching and sore throat, laryngospasm, and respiratory distress. Other β-blockers have caused mesenteric arterial thrombosis, ischemic colitis, Peyronie's disease, and erythematous rash.

Precautions and Contraindications

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

In patients with heart failure, sympathetic stimulation is vital for the support of circulatory function. Nadolol should be used with caution in patients with inadequate cardiac function, since heart failure may be precipitated by blockade of β-adrenergic stimulation when nadolol 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, nadolol 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 nadolol 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, nadolol should be discontinued, gradually if possible.

Sudden cessation of β-blocker therapy in patients with angina pectoris and/or coronary artery disease may lead to increased frequency, duration, and severity of angina episodes and, in some cases, myocardial infarction (MI) and ventricular arrhythmias. In patients without coronary artery disease, abrupt withdrawal of β-blocker therapy has also caused transient symptoms, including tremulousness, sweating, palpitation, headache, and malaise. Therefore, patients receiving nadolol (especially those with ischemic heart disease) should be warned not to interrupt or discontinue therapy without consulting their clinician. When discontinuance of long-term nadolol therapy is planned, particularly in patients with ischemic heart disease, dosage of the drug should be gradually reduced over a period of about 1-2 weeks and the patient should be carefully monitored. If exacerbation of angina occurs or acute coronary insufficiency develops after nadolol therapy is interrupted or discontinued, treatment with the drug should be reinstituted promptly, at least temporarily, and appropriate measures for the management of unstable angina pectoris should be initiated. Because coronary artery disease is common and may be unrecognized, the manufacturers caution that it may be prudent not to discontinue nadolol therapy abruptly, even in patients being treated only for hypertension.

Since β-blockers may inhibit bronchodilation produced by endogenous catecholamines, the drugs generally should not be used in patients with bronchospastic disease. Nadolol should be used with caution in patients with nonallergic bronchospasm (e.g., chronic bronchitis, emphysema). Nadolol also may interfere with the bronchodilation produced by exogenous β2-adrenergic bronchodilators.

Signs of hyperthyroidism (e.g., tachycardia) may be masked by nadolol, and patients having or suspected of developing thyrotoxicosis should be monitored closely because abrupt withdrawal of β-adrenergic blockade might precipitate thyroid storm.

It is recommended that nadolol be used with caution in patients with diabetes mellitus (especially those with labile diabetes or those prone to hypoglycemia) since the drug also may mask the signs and symptoms associated with acute hypoglycemia (e.g., tachycardia and blood pressure changes but not sweating). In addition, β-blockers also may impair glucose tolerance; delay the rate of recovery of blood glucose concentration following drug-induced hypoglycemia; alter the hemodynamic response to hypoglycemia, possibly resulting in an exaggerated hypertensive response; and possibly impair peripheral circulation. (See Cautions: Endocrine Effects.) If nadolol is used in diabetic patients receiving hypoglycemic agents, it may be necessary to adjust the dosage of the hypoglycemic agent. 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 β-blockers. In one study in nondiabetic patients, nadolol therapy did not produce changes in glucose tolerance.

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-blocking agents and may be unresponsive to usual doses of epinephrine used to treat anaphylactic reactions.

Nadolol 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. The manufacturer states that chronically administered β-blocking therapy should not be routinely withdrawn prior to major surgery; however, the decreased ability of the heart to respond to reflex β-adrenergic stimuli may increase the risks associated with general anesthesia and surgical procedures. Severe, protracted hypotension and difficulty in restarting or maintaining a heart beat have occurred during surgery in some patients who have received β-blockers. If nadolol is continued during surgery, the anesthesiologist should be informed that the patient is receiving the drug. (See Cautions: Cardiovascular Effects.)

Nadolol should be used with caution in patients with renal or hepatic impairment, and it may be necessary to reduce the dosage of the drug in those with renal impairment.

Nadolol is contraindicated in patients with bronchial asthma, sinus bradycardia and heart block greater than first degree, cardiogenic shock, or overt cardiac failure.

Pediatric Precautions

Safety and efficacy of nadolol in children have not been established.


No evidence of nadolol-induced carcinogenicity was observed in mice and rats receiving the drug orally for 2 years.

Pregnancy, Fertility, and Lactation


Nadolol has been shown to be embryotoxic and fetotoxic in rabbits, but not in rats or hamsters, when given at dosages 5-10 times the maximum recommended human dosage; no teratogenic potential was observed in any of these species. There are no adequate and well-controlled studies using nadolol in pregnant women, and the drug should be used during pregnancy only when the potential benefits justify the possible risks to the fetus. Neonates whose mothers were receiving nadolol at parturition have exhibited bradycardia, hypoglycemia, and associated symptoms.


Reproduction studies in rats using nadolol have not revealed evidence of impaired fertility.


Nadolol is distributed into milk. Because of the potential for adverse reactions to nadolol in nursing infants, a decision should be made whether to discontinue nursing or the drug, taking into account the importance of the drug to the woman.

Drug Interactions

Although some of the drug interactions that have occurred with propranolol have not been reported to date during nadolol therapy, it should be kept in mind that nadolol and propranolol have similar pharmacologic effects and probably have similar drug interactions.

Sympathomimetic Agents

The β-adrenergic stimulating effects of sympathomimetic agents are antagonized by nadolol. This interaction is especially pronounced with isoproterenol, and very large doses of isoproterenol may be needed to overcome the β-adrenergic blocking effects of nadolol. In patients receiving nadolol, epinephrine should be administered with caution since a decrease in pulse rate with first- and second-degree heart block and hypertension may occur.

Antimuscarinic Agents

Antimuscarinic agents, such as atropine, may counteract the bradycardia caused by nadolol by reestablishing the balance between sympathetic and parasympathetic actions on the heart.

Cardiovascular Drugs

When nadolol is administered with diuretics or other hypotensive drugs, the hypotensive effect of nadolol may be increased. This effect is usually used to therapeutic advantage, but careful adjustment of dosage is necessary when these drugs are used concomitantly. Phenothiazines and nadolol may have additive hypotensive activity, especially when phenothiazines are administered in large doses. In addition to its potentially additive hypotensive effect, reserpine theoretically may add to the β-adrenergic blocking activity of nadolol through its catecholamine-depleting activity, and patients receiving both drugs should be observed for hypotension and/or excessive bradycardia.

Concomitant use of β-adrenergic blocking agents (β-blockers) and certain other cardiovascular drugs (e.g., cardiac glycosides, nondihydropyridine calcium-channel blocking agents) can have additive negative effects on SA or AV nodal conduction. 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-blocker therapy.

Neuromuscular Blocking Agents

High doses of nadolol may potentiate and prolong the effects of neuromuscular blocking agents such as tubocurarine chloride.



Following oral administration of nadolol, absorption is variable and averages about 30-40% of a dose. The presence of food in the GI tract does not affect the rate or extent of absorption. After oral administration of 2 mg of nadolol (in a capsule), peak plasma concentrations usually occur in 2-4 hours. In one study in hypertensive adults who received 80 mg, 160 mg, or 320 mg of nadolol daily, mean steady-state plasma concentrations were 25.5-35.5 ng/mL, 51.7-74.1 ng/mL, and 154-191.4 ng/mL, respectively. With doses of 40-320 mg daily, the duration of nadolol's antihypertensive and antianginal effects is at least 24 hours.


Nadolol is widely distributed into body tissues. In dogs, minimal amounts of nadolol were detected in the brain and, in rats, the drug crosses the placenta. The drug is distributed into bile. Nadolol is distributed into milk.

About 30% of nadolol in serum is bound to plasma proteins.


In patients with normal renal function, the plasma half-life of nadolol is 10-24 hours and, with once-daily doses, steady-state is attained in 6-9 days. In patients with renal impairment, plasma half-life is increased.

Nadolol is not metabolized. Following oral administration of 2 mg of radiolabeled nadolol (in a capsule) in one study in patients with normal renal function, about 24.6% and 76.9% of the radioactivity was recovered in urine and feces, respectively, in 4 days. Nadolol is removed by hemodialysis.

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