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Continuing Education Activity

Nadolol is a medication used to treat angina and hypertension, which are significant risk factors for the development of coronary artery disease, heart failure, stroke, and a host of other cardiovascular conditions. Nadolol belongs to the class of beta-blocker medications. Off-labeled it is used for the management of atrial fibrillation, ventricular arrhythmias due to congenital long QT syndrome, ventricular premature beat, catecholaminergic polymorphic ventricular tachycardia, supraventricular tachycardia, gastroesophageal variceal hemorrhage prophylaxis in patients with liver cirrhosis, and thyrotoxicosis. This activity reviews the indications, mechanism of action, adverse drug reactions, toxicity, management, and contraindications for using nadolol as a valuable agent in managing hypertension, angina, and other conditions.


  • Describe the mechanism of action of nadolol.
  • Identify the most common adverse effects associated with nadolol therapy.
  • Explain the importance of monitoring patients on nadolol therapy.
  • Review the importance of improving care coordination amongst the interprofessional team members to enhance care delivery and improve outcomes for patients receiving nadolol.


FDA-labeled Indications


Nadolol has approval for long-term use in angina pectoris. Nadolol showed significant symptomatic improvement in exercise tolerance and exercise duration and was more effective than propranolol in slowing heart rate at rest and during exercise.[1]


Nadolol is a second-line agent in the treatment of hypertension. Nadolol should not be used as the first line in treating hypertension in the absence of indications to start beta-blockers. Nadolol can reduce blood pressure significantly with minimal cardio-depressant effect.[2] Adding a diuretic can enhance the effectiveness of nadolol.[3]

Non-FDA Approved Indications

Atrial Fibrillation

Nadolol can be used to attain heart rate control in the acute management of atrial fibrillation. Oral beta-blockers, including nadolol, are also widely used as the primary therapy for chronic atrial fibrillation. Nadolol also decreases relapse in patients with paroxysmal atrial fibrillation.[4]

Ventricular Arrhythmias due to Congenital Long QT Syndrome

The AHA recommends using nadolol in patients with ventricular arrhythmias due to congenital long QT syndrome to reduce adverse cardiac events and syncope and the prevention of sudden cardiac death.[5]

Ventricular Premature Beat

Nadolol is an option for the suppression of premature ventricular beats. This effect is due to bradycardia-induced prolongation of the RR interval.[6] It is more effective in patients with coronary artery disease than in patients without heart disease.[7]

Catecholaminergic Polymorphic Ventricular Tachycardia

Nadolol effectively reduces the incidence and severity of ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia. Nadolol appears to reduce ventricular arrhythmia by reducing the catecholamine effect on the beta receptor.[7] As a non-selective beta-blocker, nadolol prevents arrhythmia and cardiac arrest much more effectively than other beta-1 selective beta-blockers.[8][9]

Supraventricular Tachycardia

Nadolol is effective in the termination of acute onset supraventricular tachycardia in those patients where the vagal maneuver is not an option or failed and did not respond to adenosine.[10] Nadolol can control ventricular rate in patients with sustained response supraventricular tachycardia.[11]

Gastroesophageal Variceal Hemorrhage Prophylaxis in Patients with Liver Cirrhosis

Clinicians use nadolol to prevent and manage gastroesophageal varices and variceal hemorrhage in patients with liver cirrhosis.[12] Nadolol and other beta-blockers(e.g., propranolol) have been shown to significantly reduce variceal rebleeding, reduce deaths from variceal hemorrhage, and overall mortality.[13] In combination with isosorbide dinitrate, nadolol is very effective as prophylaxis in a patient with liver cirrhosis.[14] A multi-center trial proved that nadolol plus endoscopic variceal ligation (EVL) reduces the incidence of variceal rebleeding compared to EVL alone.[15]


Nadolol produces clinical improvement in patients with thyrotoxicosis by reducing palpitations, nervousness, and tremor. It produces this effect by reducing the level of free thyroid hormone in the bloodstream. It also reduces the T3 levels and increases the reverse T3 levels.[16]

Mechanism of Action

Nadolol is a synthetic non-selective beta-adrenergic receptor blocker and an inverse agonist.[17] It competitively blocks the beta-1 receptors in the heart and vascular smooth muscles, thus inhibiting the effect of catecholamine on these receptors without sympathomimetic or membrane-stabilizing properties, causing negative inotropic and negative chronotropic properties. This effect on vascular smooth muscle causes a reduction in peripheral vascular resistance and decreases systolic and diastolic blood pressure at rest and during exercise.[18] Its antiarrhythmic property impairs the conduction through the AV node and suppresses automaticity, thus decreasing heart rate and cardiac output at rest and during exercise. This agent’s inhibiting effect of beta-2 receptor in the juxtaglomerular apparatus results in the inhibition of renin production and subsequent reduction of angiotensinogen, angiotensin II-dependent vasoconstriction, and aldosterone-dependent water retention.


Nadolol administration is primarily through the oral route. Tablet formulations are available in 20 mg, 40 mg, 80 mg, 160 mg, 240 mg, and 320 mg strengths.

  • According to the FDA, in patients with angina pectoris and hypertension, nadolol should be started as a 40 mg once-daily oral formulation. It should be gradually increased in 40 to 80 mg increments to achieve the required therapeutic concentration and tailored to the patient’s response.[19] The maximum dosages for hypertension and angina are 320 mg and 240 mg, respectively.
  • In patients with atrial fibrillation, the American Heart Association recommends an oral dosage range of 10 mg to 240 mg to be tailored based on the patient’s response.[4]
  • In patients with catecholaminergic polymorphic ventricular tachycardia, supraventricular tachycardia, and ventricular arrhythmia due to congenital long QT syndrome, the American Heart Association recommends an oral dosage of 40 mg to 320 mg once a day.[20][21]
  • In patients with ventricular tachyarrhythmia, the American Heart Association recommends a dosage of 160 mg for long-term control.[22]
  • For both primary and secondary prophylaxis in patients with gastroesophageal variceal hemorrhage, the initial dose is 40 mg per day. This dose can increase to 80 mg per day in patients with ascites and 160 mg per day in patients without ascites. Dosing should be gradually increased every 2 to 3 days to reach a maximum tolerated dose in these patients. Heart rate should be maintained at 55 to 60 bpm, and the dosage should be stopped or decreased if the blood pressure drops below 90 mmHg.[23]
  • In patients with thyrotoxicosis, the American Thyroid Association recommends an oral dosage of 40 to 160 mg.[24]
  • The American Academy of Neurology and American Headache Society recommends an oral dosage of 40 to 160 mg once a day for prophylaxis in patients with migraines.[25]


Various animal studies in dogs and rabbits have shown that pharmacological half-life is 12 to 24 hours.[26] The inherently longer duration of action allows once-daily dosing and is as effective as propranolol with its traditional four times daily dosing.[27] Unlike other beta-blockers, nadolol is renally excreted and undergoes its first-pass metabolism in the liver. But it has little to no effect on the CYP450 system and rarely causes severe liver injury.

Specific Population

Renal Impairment: Nadolol reduces renal blood flow. Therefore, dosage intervals should require monitoring with creatinine clearance.[28] Dosage requires no modification for CrCl over 50 ml/min. Extend the dosage interval to 24 to 36 hours, 24 to 48 hours, and 40 to 60 hours for CrCl 31 to 49 ml/min/1.73 m^2, 10 to 30 ml/min/1.73 m^2, and under 10 ml/min/1.73 m^2, respectively.

Hepatic Impairment: There is no information on nadolol use in patients with hepatic impairment.

Pregnant Women: Nadolol is considered a pregnancy category C drug. Research has shown it to reduce birth weight in infants.

Breastfeeding Women: It is also contraindicated postpartum as it is expressed in breast milk. It may induce hypotension and hypoglycemia in neonates and infants.

Adverse Effects

Nadolol has been well-tolerated in most clinical studies with minimal side effects.[27] The adverse effects of nadolol are mainly because of its effect on the beta-2 receptors. There are no known reports of major organ injury from using nadolol. However, there has been evidence of a mild to moderate increase in liver enzymes in select patient populations, especially aspartate aminotransferase (AST) and alanine aminotransferase (ALT); this is because of the first-pass metabolism of nadolol in the liver. These patients are usually asymptomatic, and the liver functions return to baseline with the continuation of therapy. There is no evidence of nadolol causing clinically apparent liver injury, but this adverse effect can get aggravated when used in combination with other hepatotoxic drugs. Nadolol is safe for use in patients with cirrhosis for primary or secondary prophylaxis of varices without affecting liver function.[29]

The most common adverse effect is drowsiness and insomnia. Some other common adverse effects of nadolol are as follows:


  • AV block
  • Bradycardia
  • Hypotension
  • Raynaud phenomenon

Central Nervous System

  • Dizziness
  • Depression
  • Memory loss


  • Hepatotoxicity
  • Weakness
  • Impotence


  • Cough
  • Bronchospasm

Severe hypotension, bronchospasm, and allergic reactions are rare but life-threatening adverse effects, often necessitating immediate emergency treatment. Clinicians should not abruptly withdraw nadolol [US BOX WARNING] as it can cause rebound tachycardia, hypertension, or ischemia. Treatment should be stopped gradually to avoid these complications.[30]


Asthma/COPD: The effect of nadolol on the beta-2 receptors of the bronchial lining prevents bronchodilation and increases airway resistance, which exacerbates the effect in patients with a bronchospastic disease like asthma, thus causing wheezing and shortness of breath.[30]

Sinus Bradycardia: One known effect of nadolol is reducing the resting heart rate. In patients with low heart rates originating from sinus node dysfunction, nadolol can further reduce the rate unless a pacemaker is present.[31]

Greater than first-degree AV Block: Nadolol reduces conduction through the AV node, potentially causing an AV block. Thus, nadolol can lead to serious bradyarrhythmia in patients with partial or complete AV block. The use of other drugs that might impair AV nodal conduction can exacerbate AV blockage.[30]

Cardiogenic Shock: The combined effect of lowering the resting heart rate and increasing the AV nodal conduction delay can potentially aggravate the already reduced cardiac output in patients with cardiogenic shock.[30]

Decompensated Cardiac Failure: Beta-blockers are a cornerstone in the long-term treatment of compensated chronic heart failure with reduced ejection fraction. It reduces the detrimental effect of sympathetic drive on the heart. However, nadolol is contraindicated in patients with uncompensated heart failure. These patients rely on catecholamines for sustaining their heart rate and cardiac output, and nadolol in these patients can exacerbate the symptoms of heart failure.[30]

Pregnancy and Breastfeeding: For managing hypertension during pregnancy, beta-blockers like labetalol are preferable to nadolol.[30]

Hypersensitivity to nadolol.

Anesthetic agents that can cause myocardial depression.


Heart Rate: The clinical team should maintain the patient's heart rate above 55 bpm in patients taking nadolol. The heart rate specifically requires monitoring while escalating the dose, which can cause further bradycardia, and while withdrawing the medications, it can cause rebound tachycardia.[31]

Blood Pressure: The blood pressure should be maintained above 90 mmHg systolic, especially while escalating and withdrawing the medication.[30]

Signs and symptoms of Exacerbation: Abrupt withdrawal of nadolol can cause rebound tachycardia and reduced blood flow to the myocardial tissue, generating anginal symptoms or worsening angina.[30]


Most nadolol poisonings occur via the intentional consumption of the tablet. There are no reports of significant toxicity in the literature.[27] Most cases of nadolol poisoning are mild. These patients can be observed in an emergency department for 4 hours and discharged if no signs of poisoning develop. If there is moderate to severe toxicity, early decontamination with activated charcoal can be used along with gastric lavage if significant ingestion is suspected. After stabilizing the patient for airway, breathing, and circulation, enhanced elimination with hemodialysis is possible, considering the low volume of distribution and longer half-life of nadolol.[30]

Signs and symptoms of moderate to severe poisoning include severe hypotension, bradycardia, bronchospasm, heart failure, hypoglycemia, seizure, and coma. First, maintaining a patent airway is essential. Use suction if necessary, attempt to maintain oxygen saturation above 90%, and resort to endotracheal intubation if necessary. Continuously monitor the patient for pulmonary edema or signs of shock. There is no specific antidote for nadolol toxicity. However, for the treatment of hypotension, glucagon, dopamine, or sodium bicarbonate, followed by multiple IV boluses of epinephrine if the former is not adequate, can be used.[32] Glucagon increases cAMP via a non-catecholamine mechanism, and thus, it can produce both ionotropic and chronotropic effects. For bradycardia, atropine is the therapy of choice; if the heart rate remains low after that, then IV isoproterenol or cardiac pacing can be done.[30] 

Treat heart failure with cardiac glycosides and diuretics.[30] Treat bronchospasm with nebulized beta-agonists (albuterol). Please note that higher than usual or multiple doses may be necessary.[30] Treat beta-blocker-induced anaphylaxis with a lower-than-usual dose of epinephrine, as the unopposed alpha-receptor effect can cause coronary vasoconstriction and paradoxical hypertension.

Enhancing Healthcare Team Outcomes

The primary use of nadolol is in the treatment of angina and hypertension.[33][2] While the drug is safe, its use still requires monitoring.

Interprofessional healthcare team members, including clinicians, nurses, and pharmacists, should be cautious while withdrawing or stopping the drug as it can cause life-threatening rebound hypertension, tachycardia, and signs and symptoms of angina. Nadolol should be used cautiously with diuretics as it can potentiate the effect of hypotension by nadolol.[3] It is worth noting that nadolol can enhance and potentiate the effect of the neuromuscular blocking agent tubocurarine chloride. Improved treatment outcome with nadolol is achievable with enhanced team performance by ordering appropriate follow-up and monitoring for signs of inadequate dosage or symptoms of toxicity.

To improve outcomes and lower morbidity, the pharmacist should educate the patient on medication compliance and avoid using other drugs/herbs without consulting the physician. The pharmacist should also perform medication reconciliation to monitor any potential interactions and report these to the rest of the healthcare team. Nursing staff will have more frequent contact with patients and should gauge treatment success and observe for adverse effects. These factors must get communicated to the prescribing clinicians for dose and/or drug changes to the therapy regimen. Nadolol therapy requires the efforts of an interprofessional healthcare team, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to achieve optimal patient results and minimize adverse events. [Level 5]



Shwetha Gopal


2/10/2023 6:21:48 PM



Turner GG, Nelson RR, Nordstrom LA, Diefenthal HC, Gobel FL. Comparative effect of nadolol and propranolol on exercise tolerance in patients with angina pectoris. British heart journal. 1978 Dec:40(12):1361-70     [PubMed PMID: 32899]

Level 2 (mid-level) evidence


Weber MA, Schiffrin EL, White WB, Mann S, Lindholm LH, Kenerson JG, Flack JM, Carter BL, Materson BJ, Ram CV, Cohen DL, Cadet JC, Jean-Charles RR, Taler S, Kountz D, Townsend RR, Chalmers J, Ramirez AJ, Bakris GL, Wang J, Schutte AE, Bisognano JD, Touyz RM, Sica D, Harrap SB. Clinical practice guidelines for the management of hypertension in the community: a statement by the American Society of Hypertension and the International Society of Hypertension. Journal of clinical hypertension (Greenwich, Conn.). 2014 Jan:16(1):14-26. doi: 10.1111/jch.12237. Epub 2013 Dec 17     [PubMed PMID: 24341872]

Level 1 (high-level) evidence


Volicer L, Liang CS, Gavras H, Tifft CP, Kershaw GR, Gavras I, Griffith DL, Vukovitch R, Brunner HR. Effect of nadolol in treatment of hypertension. Journal of clinical pharmacology. 1979 Feb-Mar:19(2-3):137-47     [PubMed PMID: 33998]


January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, Conti JB, Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG, Tchou PJ, Tracy CM, Yancy CW, ACC/AHA Task Force Members. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation. 2014 Dec 2:130(23):e199-267. doi: 10.1161/CIR.0000000000000041. Epub 2014 Mar 28     [PubMed PMID: 24682347]

Level 1 (high-level) evidence


Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology. 2018 Oct 2:72(14):e91-e220. doi: 10.1016/j.jacc.2017.10.054. Epub 2018 Aug 16     [PubMed PMID: 29097296]

Level 1 (high-level) evidence


Pitzalis MV, Mastropasqua F, Massari F, Passantino A, Luzzi G, Forleo C, Rizzon P. Effects of nadolol and its combination with atrial pacing on rate-enhanced ventricular premature complexes. The American journal of cardiology. 1996 Nov 15:78(10):1177-9     [PubMed PMID: 8914889]


Pitzalis MV, Mastropasqua F, Massari F, Totaro P, Passantino A, Rizzon P. The effect of nadolol on heart rate and the standard deviation of the RR intervals. European heart journal. 1995 Feb:16(2):269-75     [PubMed PMID: 7744100]


Hayashi M, Denjoy I, Extramiana F, Maltret A, Buisson NR, Lupoglazoff JM, Klug D, Hayashi M, Takatsuki S, Villain E, Kamblock J, Messali A, Guicheney P, Lunardi J, Leenhardt A. Incidence and risk factors of arrhythmic events in catecholaminergic polymorphic ventricular tachycardia. Circulation. 2009 May 12:119(18):2426-34. doi: 10.1161/CIRCULATIONAHA.108.829267. Epub 2009 Apr 27     [PubMed PMID: 19398665]


Leren IS, Saberniak J, Majid E, Haland TF, Edvardsen T, Haugaa KH. Nadolol decreases the incidence and severity of ventricular arrhythmias during exercise stress testing compared with β1-selective β-blockers in patients with catecholaminergic polymorphic ventricular tachycardia. Heart rhythm. 2016 Feb:13(2):433-40. doi: 10.1016/j.hrthm.2015.09.029. Epub 2015 Sep 30     [PubMed PMID: 26432584]


Olukotun AY, Klein GJ. Efficacy and safety of intravenous nadolol for supraventricular tachycardia. The American journal of cardiology. 1987 Aug 31:60(6):59D-62D     [PubMed PMID: 3630923]


Chang MS, Sung RJ, Tai TY, Lin SL, Liu PH, Chiang BN. Nadolol and supraventricular tachycardia: an electrophysiologic study. Journal of the American College of Cardiology. 1983 Nov:2(5):894-903     [PubMed PMID: 6138376]


Garcia-Tsao G, Sanyal AJ, Grace ND, Carey W, Practice Guidelines Committee of the American Association for the Study of Liver Diseases, Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology (Baltimore, Md.). 2007 Sep:46(3):922-38     [PubMed PMID: 17879356]


Hayes PC, Davis JM, Lewis JA, Bouchier IA. Meta-analysis of value of propranolol in prevention of variceal haemorrhage. Lancet (London, England). 1990 Jul 21:336(8708):153-6     [PubMed PMID: 1973480]

Level 1 (high-level) evidence


Merkel C, Marin R, Sacerdoti D, Donada C, Cavallarin G, Torboli P, Amodio P, Sebastianelli G, Bolognesi M, Felder M, Mazzaro C, Gatta A. Long-term results of a clinical trial of nadolol with or without isosorbide mononitrate for primary prophylaxis of variceal bleeding in cirrhosis. Hepatology (Baltimore, Md.). 2000 Feb:31(2):324-9     [PubMed PMID: 10655253]


de la Peña J, Brullet E, Sanchez-Hernández E, Rivero M, Vergara M, Martin-Lorente JL, Garcia Suárez C. Variceal ligation plus nadolol compared with ligation for prophylaxis of variceal rebleeding: a multicenter trial. Hepatology (Baltimore, Md.). 2005 Mar:41(3):572-8     [PubMed PMID: 15726659]

Level 1 (high-level) evidence


Peden NR, Isles TE, Stevenson IH, Crooks J. Nadolol in thyrotoxicosis. British journal of clinical pharmacology. 1982 Jun:13(6):835-40     [PubMed PMID: 6124267]


Khilnani G, Khilnani AK. Inverse agonism and its therapeutic significance. Indian journal of pharmacology. 2011 Sep:43(5):492-501. doi: 10.4103/0253-7613.84947. Epub     [PubMed PMID: 22021988]


Hornung RS, Gould BA, Kieso H, Raftery EB. A study of nadolol to determine its effect on ambulatory blood pressure over 24 hours, and during exercise testing. British journal of clinical pharmacology. 1982 Jul:14(1):83-8     [PubMed PMID: 6125200]


Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC Jr, Spencer CC, Stafford RS, Taler SJ, Thomas RJ, Williams KA Sr, Williamson JD, Wright JT Jr. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology. 2018 May 15:71(19):2199-2269. doi: 10.1016/j.jacc.2017.11.005. Epub 2017 Nov 13     [PubMed PMID: 29146533]

Level 3 (low-level) evidence


Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: Executive summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart rhythm. 2018 Oct:15(10):e190-e252. doi: 10.1016/j.hrthm.2017.10.035. Epub 2017 Oct 30     [PubMed PMID: 29097320]

Level 1 (high-level) evidence


Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NA 3rd, Field ME, Goldberger ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky B, Russo AM, Shen WK, Tracy CM, Al-Khatib SM, Evidence Review Committee Chair‡. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2016 Apr 5:133(14):e471-505. doi: 10.1161/CIR.0000000000000310. Epub 2015 Sep 23     [PubMed PMID: 26399662]

Level 1 (high-level) evidence


Nademanee K, Schleman MM, Singh BN, Morganroth J, Reid PR, Stritar JA. Beta-adrenergic blockade by nadolol in control of ventricular tachyarrhythmias. American heart journal. 1984 Oct:108(4 Pt 2):1109-15     [PubMed PMID: 6207720]


Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the American Association for the study of liver diseases. Hepatology (Baltimore, Md.). 2017 Jan:65(1):310-335. doi: 10.1002/hep.28906. Epub 2016 Dec 1     [PubMed PMID: 27786365]


Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, Rivkees SA, Samuels M, Sosa JA, Stan MN, Walter MA. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid : official journal of the American Thyroid Association. 2016 Oct:26(10):1343-1421     [PubMed PMID: 27521067]


Silberstein SD, Holland S, Freitag F, Dodick DW, Argoff C, Ashman E, Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Evidence-based guideline update: pharmacologic treatment for episodic migraine prevention in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology. 2012 Apr 24:78(17):1337-45. doi: 10.1212/WNL.0b013e3182535d20. Epub     [PubMed PMID: 22529202]

Level 2 (mid-level) evidence


Tan HJ, Ling WC, Chua AL, Lee SK. Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2021 Sep:90():153623. doi: 10.1016/j.phymed.2021.153623. Epub 2021 Jun 11     [PubMed PMID: 34303263]


Heel RC, Brogden RN, Pakes GE, Speight TM, Avery GS. Nadolol: a review of its pharmacological properties and therapeutic efficacy in hypertension and angina pectoris. Drugs. 1980 Jul:20(1):1-23     [PubMed PMID: 6105067]


Herrera J, Vukovich RA, Griffith DL. Elimination of nadolol by patients with renal impairment. British journal of clinical pharmacology. 1979:7 Suppl 2(Suppl 2):227S-231S     [PubMed PMID: 37878]


Merkel C, Sacerdoti D, Finucci GF, Zuin R, Bazzerla G, Bolognesi M, Gatta A. Effect of nadolol on liver haemodynamics and function in patients with cirrhosis. British journal of clinical pharmacology. 1986 Jun:21(6):713-9     [PubMed PMID: 3741719]


. Nadolol (Corgard) - a new beta-blocker. The Medical letter on drugs and therapeutics. 1980 Apr 18:22(8):33-4     [PubMed PMID: 6102734]

Level 3 (low-level) evidence


Hitzenberger G. Initial experience with a new long-acting beta-blocker, nadolol, in hypertensive patients. The Journal of international medical research. 1979:7(1):33-8     [PubMed PMID: 33862]


Ehgartner GR, Zelinka MA. Hemodynamic instability following intentional nadolol overdose. Archives of internal medicine. 1988 Apr:148(4):801-2     [PubMed PMID: 3355299]


Burr DC, Ross J. How does binocular delay give information about depth? Vision research. 1979:19(5):523-32     [PubMed PMID: 483580]