Jump to content

Beta blocker

From Wikipedia, the free encyclopedia
(Redirected fromBeta-adrenergic blocker)

Beta blockers
Drug class
Propranolol
Skeletal formulaofpropranolol,the first clinically successful beta blocker.
Class identifiers
Synonymsbeta-blockers, β-blockers, beta-adrenergic blocking agents, beta antagonists, beta-adrenergic antagonists, beta-adrenoreceptor antagonists, beta adrenergic receptor antagonists, BB
UseHypertension,arrhythmia,etc.
ATC codeC07
Biological targetbeta receptors
Clinical data
Drugs.comDrug Classes
Consumer ReportsBest Buy Drugs
WebMDMedicineNetRxList
External links
MeSHD000319
Legal status
In Wikidata

Beta blockers,also spelledβ-blockers,are a class of medications that are predominantly used to manage abnormal heart rhythms (arrhythmia), and to protect the heart from a secondheart attackafter a first heart attack (secondary prevention).[1]They are also widely used to treathigh blood pressure,although they are no longer the first choice for initial treatment of most patients.[2]

Beta blockers arecompetitive antagoniststhat block the receptor sites for theendogenouscatecholaminesepinephrine(adrenaline) andnorepinephrine(noradrenaline) onadrenergic beta receptors,of thesympathetic nervous system,which mediates thefight-or-flight response.[3]: 152 [4]Some block activation of all types ofβ-adrenergic receptorsand others are selective for one of the three known types of beta receptors, designated β1,β2and β3receptors.[3]: 153 β1-adrenergic receptorsare located mainly in the heart and in the kidneys.[4]β2-adrenergic receptorsare located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.[4]β3-adrenergic receptorsare located in fat cells.[5]

Beta receptors are found on cells of theheartmuscles,smooth muscles,airways,arteries,kidneys,and other tissues that are part of thesympathetic nervous systemand lead to stress responses, especially when they are stimulated byepinephrine(adrenaline). Beta blockers interfere with the binding to the receptor of epinephrine and other stress hormones and weaken the effects of stress hormones.

In 1964,James Black[6]synthesized the first clinically significant beta blockers—propranololandpronethalol;it revolutionized the medical management ofangina pectoris[7]and is considered by many to be one of the most important contributions to clinical medicine andpharmacologyof the 20th century.[8]

For the treatment of primary hypertension,meta-analysesof studies which mostly usedatenololhave shown that although beta blockers are more effective thanplaceboin preventingstrokeand total cardiovascular events, they are not as effective asdiuretics,medications inhibiting therenin–angiotensin system(e.g.,ACE inhibitors), orcalcium channel blockers.[9][10][11][12]

Medical uses

[edit]

Beta blockers are utilized in the treatment of various conditions related to the heart and vascular system, as well as several other medical conditions. Common heart-related conditions for which beta blockers are well-established include angina pectoris, acute coronary syndromes, hypertension, and arrhythmias such as atrial fibrillation and heart failure. They are also used in the management of other heart diseases, such as hypertrophic obstructive cardiomyopathy, mitral valve stenosis or prolapse, and dissecting aneurysm. Additionally, beta blockers find applications in vascular surgery, the treatment of anxiety states, cases of thyrotoxicosis, glaucoma, migraines, and esophageal varices.[13]

Congestive heart failure

[edit]

Although beta blockers were once contraindicated incongestive heart failure,as they have the potential to worsen the condition due to their effect of decreasing cardiac contractility, studies in the late 1990s showed their efficacy at reducing morbidity and mortality.[14][15][16]Bisoprolol,carvedilol,and sustained-releasemetoprololare specifically indicated as adjuncts to standardACE inhibitoranddiuretictherapy in congestive heart failure, although at doses typically much lower than those indicated for other conditions. Beta blockers are only indicated in cases of compensated, stable congestive heart failure; in cases of acute decompensated heart failure, beta blockers will cause a further decrease in ejection fraction, worsening the patient's current symptoms.[citation needed]

Beta blockers are known primarily for their reductive effect on heart rate, although this is not the only mechanism of action of importance in congestive heart failure.[17]Beta blockers, in addition to their sympatholytic β1activity in the heart, influence therenin–angiotensin systemat the kidneys. Beta blockers cause a decrease inreninsecretion, which in turn reduces the heart oxygen demand by lowering theextracellularvolume and increasing the oxygen-carrying capacity of the blood. Heart failure characteristically involves increased catecholamine activity on the heart, which is responsible for several deleterious effects, including increased oxygen demand, propagation of inflammatory mediators, and abnormal cardiac tissue remodeling, all of which decrease the efficiency of cardiac contraction and contribute to the low ejection fraction.[18]Beta blockers counter this inappropriately high sympathetic activity, eventually leading to an improved ejection fraction, despite an initial reduction in ejection fraction.[citation needed]

Trials have shown beta blockers reduce the absolute risk of death by 4.5% over a 13-month period. In addition to reducing the risk of mortality, the numbers of hospital visits and hospitalizations were also reduced in the trials.[19]A 2020 Cochrane review found minimal evidence to support the use of beta blockers in congestive heart failure in children, however did identify that from the data available, that they may be of benefit.[20]

Therapeutic administration of beta blockers for congestive heart failure ought to begin at very low doses (1⁄8of target) with a gradual escalation of the dose. The heart of the patient must adjust to decreasing stimulation by catecholamines and find a new equilibrium at a lower adrenergic drive.[21]

Acute myocardial infarction

[edit]

Beta blockers are indicated for the treatment of acutemyocardial infarctions.During a myocardial infarction, systemic stress causes an increase in circulatingcatecholamines.[22][23]This results an increase in heart rate and blood pressure, therefore increasing myocardial oxygen demand.[23][22]Beta blockers competitively inhibit catecholamines acting on the β1-adrenergic receptors, thus reducing these detrimental effects and resulting in reduced myocardial oxygen consumption and demand.[22]

A 2019 Cochrane review compared beta blockers withplaceboor no intervention, it found that beta blockers probably reduced the short-term risk of reinfarction and the long-term risk ofall-cause mortalityand cardiovascular mortality.[22]The review identified that beta blockers likely had little to no impact on short-term all-cause mortality and cardiovascular mortality.[22]

Hypertension

[edit]

Beta blockers are widely used for the treatment of hypertension.[24]

A 2014 Cochrane review found that in individuals with mild-to-moderate hypertension, non-selective beta blockers led to a reduction of -10/-7mmHg (systolic/diastolic) without increased rates of adverse events.[25]At higher doses, it was found to increase the rate of adverse effects such as a reduction in heart rate, without a corresponding reduction in blood pressure.[25]

A 2017 Cochrane review on the use of beta blockers in hypertension found a modest reduction in cardiovascular disease but little to no change in mortality[26]It suggested that the effects of beta blockers are inferior to other anti-hypertensive medications.[26]

Anxiety

[edit]

Officially, beta blockers are not approved foranxiolyticuse by the U.S.Food and Drug Administration.[27]However, many controlled trials in the past 25 years indicate beta blockers are effective inanxiety disorders,though the mechanism of action is not known.[28]The physiological symptoms of thefight-or-flightresponse (pounding heart, cold/clammy hands, increased respiration, sweating, etc.) are significantly reduced, thus enabling anxious individuals to concentrate on the task at hand.[citation needed]

Musicians, public speakers, actors, and professionaldancershave been known to use beta blockers to avoidperformance anxiety,stage fright,and tremor during bothauditionsand public performances. The application to stage fright was first recognized inThe Lancetin 1976, and by 1987, a survey conducted by theInternational Conference of Symphony Orchestra Musicians,representing the 51 largest orchestras in the United States, revealed 27% of its musicians had used beta blockers and 70% obtained them from friends, not physicians.[29]Beta blockers are inexpensive, said to be relatively safe, and on one hand, seem to improve musicians' performances on a technical level, while some, such as Barry Green, the author of "The Inner Game of Music" and Don Greene, a former Olympic diving coach who teaches Juilliard students to overcome their stage fright naturally, say the performances may be perceived as "soulless and inauthentic".[29]

Surgery

[edit]

Low certainty evidence indicates that the use of beta blockers around the time of cardiac surgery may decrease the risk ofheart dysrhythmiasandatrial fibrillation.[30]Starting them around the time of other types of surgery, however, may worsen outcomes. For non-cardiac surgery, the use of beta blockers to prevent adverse effects may reduce the risk of atrial fibrillation and myocardial infarctions (very low certainty evidence), however, there is moderate certainty evidence that this approach may increase the risk of hypotension.[31]Low-certainty evidence suggests that beta blockers used perioperatively in non-cardiac surgeries may increase the risk of bradycardia.[31]

Other

[edit]

A 2014 Cochrane review investigated the use of beta blockers in the maintenance of chronic type B thoracicaortic aneurysmin comparison to other anti hypertensive medications.[32]The review found no suitable evidence to support the current guidelines recommending its use.[32]

A 2017 Cochrane review on the use of beta blockers to prevent aortic dissections in people with Marfan syndrome was unable to draw definitive conclusions due to lack of evidence.[33]

Performance-enhancing use

[edit]

Because they promote lower heart rates and reduce tremors, beta blockers have been used in professional sports where high accuracy is required, includingarchery,shooting,golf[34]andsnooker.[34]Beta blockers are banned in some sports by theInternational Olympic Committee.[35]In the2008 Summer Olympics,50-metre pistolsilver medalist and10-metre air pistolbronze medalistKim Jong-sutested positive forpropranololand was stripped of his medals.[36]

For similar reasons, beta blockers have also been used by surgeons.[37]

Classical musicians have commonly used beta blockers since the 1970s to reducestage fright.[38]

Adverse effects

[edit]

Adverse drug reactionsassociated with the use of beta blockers include:nausea,diarrhea,bronchospasm,dyspnea,cold extremities, exacerbation ofRaynaud's syndrome,bradycardia,hypotension,heart failure,heart block,fatigue,dizziness,alopecia(hair loss), abnormal vision,hallucinations,insomnia,nightmares,sexual dysfunction,erectile dysfunction,alteration ofglucoseandlipid metabolism.[medical citation needed]Mixed α1/β-antagonist therapy is also commonly associated withorthostatic hypotension. Carvediloltherapy is commonly associated withedema.[39][page needed] Due to the high penetration across theblood–brain barrier,lipophilic beta blockers, such aspropranololandmetoprolol,are more likely than other less lipophilic beta blockers to cause sleep disturbances, such as insomnia, vivid dreams and nightmares.[40]

Adverse effects associated with β2-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with β1-selective (often termed "cardioselective" ) agents, but receptor selectivity diminishes at higher doses. Beta blockade, especially of the beta-1 receptor at themacula densa,inhibits renin release, thus decreasing the release ofaldosterone.This causeshyponatremiaandhyperkalemia.[citation needed]

Hypoglycemiacan occur with beta blockade because β2-adrenoceptors normally stimulateglycogenbreakdown (glycogenolysis) in the liver and pancreatic release of thehormoneglucagon,which work together to increase plasma glucose. Therefore, blocking β2-adrenoceptors lowers plasma glucose. β1-blockers have fewer metabolic side effects in diabetic patients; however, the fast heart rate that serves as a warning sign for insulin-induced low blood sugar may be masked, resulting inhypoglycemia unawareness.This is termedbeta blocker-induced hypoglycemia unawareness.Therefore, beta blockers are to be used cautiously in diabetics.[41]

A 2007 study revealed diuretics and beta blockers used for hypertension increase a patient's risk of developingdiabetes mellitus,whileACE inhibitorsandangiotensin II receptor antagonists(angiotensin receptor blockers) actually decrease the risk of diabetes.[42]Clinical guidelines in Great Britain, but not in the United States, call for avoiding diuretics and beta blockers as first-line treatment of hypertension due to the risk of diabetes.[43]

Beta blockers must not be used in the treatment of selective alpha-adrenergic agonist overdose. The blockade of only beta receptors increasesblood pressure,reduces coronary blood flow, leftventricular function,andcardiac outputand tissue perfusion by means of leaving the alpha-adrenergic system stimulation unopposed.[medical citation needed]Beta blockers with lipophilic properties and CNS penetration such asmetoprololandlabetalolmay be useful for treating CNS and cardiovascular toxicity from a methamphetamine overdose.[44]The mixedalpha-and beta blocker labetalol is especially useful for treatment of concomitant tachycardia and hypertension induced by methamphetamine.[45]The phenomenon of "unopposed alpha stimulation" has not been reported with the use of beta blockers for treatment of methamphetamine toxicity.[45]Other appropriateantihypertensivedrugs to administer during hypertensive crisis resulting from stimulant overdose arevasodilatorssuch asnitroglycerin,diureticssuch asfurosemide,andalpha blockerssuch asphentolamine.[46]

Contraindications and cautions

[edit]
Absolute contraindications:

Relative contraindications, or contraindications specific to certain beta-blockers:

  • Long QT syndrome: sotalol is contraindicated
  • History oftorsades de pointes:sotalol is contraindicated

Cautions:

Asthma

[edit]

The 2007 National Heart, Lung, and Blood Institute (NHLBI) asthma guidelines recommend against the use of non-selective beta blockers in asthmatics, while allowing for the use of cardio selective beta blockers.[48]: 182 

Cardio selective beta blocker (β1blockers) can be prescribed at the least possible dose to those with mild to moderate respiratory symptoms.[49][50]β2-agonistscan somewhat mitigate β-blocker-inducedbronchospasmwhere it exerts greater efficacy on reversingselectiveβ-blocker-induced bronchospasm than thenonselectiveβ-blocker-induced worsening asthma and/or COPD.[49]

Diabetes mellitus

[edit]

Epinephrine signals early warning of the upcominghypoglycemia.[51]

Beta blockers' inhibition on epinephrine's effect can somewhat exacerbate hypoglycemia by interfering withglycogenolysisand mask signs of hypoglycemia such as tachycardia, palpitations,diaphoresis,and tremors. Diligent blood glucose level monitoring is necessary for a patient with diabetes mellitus on beta blocker.

Hyperthyroidism

[edit]

Abrupt withdrawal can result in athyroid storm.[47]

Bradycardia or AV block

[edit]

Unless a pacemaker is present, beta blockers can severely depress conduction in the AV node, resulting in a reduction of heart rate and cardiac output. One should be very cautious with the use of beta blockers in tachycardia patients with Wolff-Parkinson-White Syndrome, as it can result in life-threatening arrhythmia in certain patients. By slowing the conduction through the AV node, preferential conduction through the accessory pathway is favored. If the patient happens to develop atrial flutter, this could lead to a 1:1 conduction with very fast ventricular rate, or worse, ventricular fibrillation in the case of atrial fibrillation.[citation needed]

Toxicity

[edit]

Glucagon,used in the treatment of overdose,[52][53]increases the strength of heart contractions, increases intracellularcAMP,and decreases renalvascular resistance.It is, therefore, useful in patients with beta blocker cardiotoxicity.[54][55]Cardiac pacingis usually reserved for patients unresponsive topharmacological therapy.

People experiencing bronchospasm due to the β2receptor-blocking effects of nonselective beta blockers may be treated withanticholinergicdrugs, such asipratropium,which are safer thanbeta agonistsin patients withcardiovascular disease.Other antidotes for beta blocker poisoning aresalbutamolandisoprenaline.

Pharmacology

[edit]

Intrinsic sympathomimetic activity

[edit]

Also referred to as intrinsic sympathomimetic effect, this term is used particularly with beta blockers that can show both agonism and antagonism at a given beta receptor, depending on the concentration of the agent (beta blocker) and the concentration of the antagonized agent (usually an endogenous compound, such as norepinephrine). Seepartial agonistfor a more general description.[citation needed]

Some beta blockers (e.g.oxprenolol,pindolol,penbutolol,labetalolandacebutolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low-levelagonistactivity at the β-adrenergic receptor while simultaneously acting as a receptor siteantagonist.These agents, therefore, may be useful in individuals exhibiting excessivebradycardiawith sustained beta blocker therapy.[citation needed]

Agents with ISA should not be used for patients with any kind of angina as it can aggravate or after myocardial infarctions. They may also be less effective than other beta blockers in the management ofanginaandtachyarrhythmia.[39]

β-Adrenergic receptor antagonism

[edit]

Stimulation of β1receptors by epinephrine and norepinephrine induces a positivechronotropicandinotropiceffect on the heart and increases cardiac conduction velocity and automaticity.[56]Stimulation of β1receptors on the kidney causesreninrelease.[57]Stimulation of β2receptors inducessmooth musclerelaxation,[58]induces tremor inskeletal muscle,[59]and increasesglycogenolysisin theliverandskeletal muscle.[60]Stimulation of β3receptors induceslipolysis.[61]

Beta blockers inhibit these normal epinephrine- and norepinephrine-mediatedsympatheticactions,[3]but have minimal effect on resting subjects.[citation needed] That is, they reduce the effect of excitement or physical exertion on heart rate and force of contraction,[62]and also tremor,[63]and breakdown of glycogen. Beta blockers can have a constricting effect on the bronchi of the lungs, possibly worsening or causing asthma symptoms.[64]

Since β2adrenergic receptors can cause vascular smooth muscle dilation, beta blockers may cause some vasoconstriction. However, this effect tends to be small because the activity of β2receptors is overshadowed by the more dominant vasoconstricting α1receptors. By far the greatest effect of beta blockers remains in the heart. Newer, third-generation beta blockers can cause vasodilation through blockade of alpha-adrenergic receptors.[65]

Accordingly, nonselective beta blockers are expected to have antihypertensive effects.[66]The primary antihypertensive mechanism of beta blockers is unclear, but may involve reduction in cardiac output (due to negative chronotropic and inotropic effects).[67]It may also be due to reduction in renin release from the kidneys, and acentral nervous systemeffect to reduce sympathetic activity (for those beta blockers that do cross theblood–brain barrier,e.g. propranolol).[citation needed]

Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand. Negativechronotropicproperties of beta blockers allow the lifesaving property of heart rate control. Beta blockers are readily titrated to optimal rate control in many pathologic states.[citation needed]

The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade—resulting in depression ofsinus nodefunction andatrioventricular nodeconduction, and prolongedatrialrefractory periods.Sotalol,in particular, has additional antiarrhythmic properties and prolongsaction potentialduration throughpotassium channelblockade.

Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via therenin–angiotensin–aldosterone system,with a resultant decrease in blood pressure due to decreased sodium and water retention.

α1-Adrenergic receptor antagonism

[edit]

Some beta blockers (e.g.,labetalolandcarvedilol) exhibit mixed antagonism of both β- and α1-adrenergic receptors,which provides additionalarteriolarvasodilating action.[68][69]

Blood–brain barrier permeability

[edit]

Beta blockers vary in theirlipophilicity(fat solubility) and in turn in their ability to cross theblood–brain barrierand exert effects in thecentral nervous system.[70]Beta blockers with greater blood–brain barrierpermeabilitycan have bothneuropsychiatrictherapeutic benefits andside effects,as well as adversecognitiveeffects.[70]Central nervous system-related side effects and risks of beta blockers may includefatigue,depression,sleep disorders(namelyinsomnia) andnightmares,visual hallucinations,delirium,psychosis,Parkinson's disease,andfalling.[70]Conversely, central nervous system-related benefits of beta blockers may include prevention and treatment ofmigraine,essential tremor,akathisia,anxiety,post-traumatic stress disorder,aggression,andobsessive–compulsive disorder.[70]

Most beta blockers are lipophilic and can cross into the brain, but there are a number of exceptions.[70]Highly lipophilic beta blockers includepenbutolol,pindolol,propranolol,andtimolol,moderately lipophilic beta blockers includeacebutolol,betaxolol,bisoprolol,carvedilol,metoprolol,andnebivolol,and low lipophilicity or hydrophilic beta blockers includeatenolol,carteolol,esmolol,labetalol,nadolol,andsotalol.[70]It is thought that highly lipophilic beta blockers are able to readily cross into the brain, moderately lipophilic beta blockers are able to cross to a lesser degree, and low lipophilicity or hydrophilic beta blockers are minimally able to cross.[70]More lipophilic beta-blockers are known to suppress melatonin release by 50-80%.[71][72][73]The preceding beta blockers also vary in theirintrinsic sympathomimetic activityandβ1-adrenergic receptorselectivity(or cardioselectivity), resulting in further differences in pharmacological profiles and suitability in different contexts between them.[70]

Agents

[edit]
Dichloroisoprenaline,the first beta blocker

Nonselective agents

[edit]

Nonselective beta blockers display both β1and β2antagonism.[74]

β1-selective agents

[edit]

β1-selective beta blockers are also known as cardioselective beta blockers.[74]Pharmacologically, the beta-blockade of the β1receptors in the heart will act oncAMP.The function of cAMP as a second messenger in the cardiac cell is that it phosphorylates theLTCCand theryanodine receptorto increase intracellular calcium levels and cause contraction. Beta-blockade of the β1receptor will inhibit cAMP from phosphorylating, and it will decrease the ionotrophic and chronotropic effect. Note that drugs may be cardioselective, or act on β1receptors in the heart only, but still have instrinsic sympathomimetic activity.

Nebivolol and bisoprolol are the most β1cardioselective beta blockers.[80]

β2-selective agents

[edit]

β3-selective agents

[edit]

β1selective antagonist and β3agonist agents

[edit]

Comparative information

[edit]

Pharmacological differences

[edit]
  • Agents with intrinsic sympathomimetic action (ISA)
  • Agents organized by lipid solubility (lipophilicity)[86]
    • High lipophilicity: propranolol, labetalol
    • Intermediate lipophilicity: metoprolol, bisoprolol, carvedilol, acebutolol, timolol, pindolol
    • Low lipophilicity (also known as hydrophilic beta blockers): atenolol, nadolol, and sotalol
  • Agents withmembrane stabilizing effect[87]
    • Carvedilol, propranolol > oxprenolol > labetalol, metoprolol, timolol

Indication differences

[edit]

Propranololis the only agent indicated for the control of tremor, portal hypertension, and esophageal variceal bleeding, and used in conjunction with α-blocker therapy inphaeochromocytoma.[39]

Other effects

[edit]

Beta blockers, due to their antagonism at beta-1 adrenergic receptors, inhibit both the synthesis of newmelatoninand its secretion by thepineal gland.The neuropsychiatric side effects of some beta blockers (e.g. sleep disruption,insomnia) may be due to this effect.[93]

Some pre-clinical and clinical research suggests that some beta blockers may be beneficial for cancer treatment.[94][95]However, other studies do not show a correlation between cancer survival and beta blocker usage.[96][97]Also, a 2017 meta-analysis failed to show any benefit for the use of beta blockers in breast cancer.[98]

Beta blockers have also been used for the treatment ofschizoid personality disorder.[99]However, there is limited evidence supporting the efficacy of supplemental beta blocker use in addition to antipsychotic drugs for treating schizophrenia.[100][101]

Contrast agentsare not contraindicated in those receiving beta blockers.[102]

See also

[edit]

References

[edit]
  1. ^Freemantle N, Cleland J, Young P, Mason J, Harrison J (June 1999)."beta Blockade after myocardial infarction: systematic review and meta regression analysis".BMJ.318(7200): 1730–1737.doi:10.1136/bmj.318.7200.1730.PMC31101.PMID10381708.
  2. ^James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, et al. (February 2014)."2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8)".JAMA.311(5): 507–520.doi:10.1001/jama.2013.284427.PMID24352797.
  3. ^abcFrishman WH, Cheng-Lai A, Nawarskas J, eds. (2005)."Beta-Adrenergic Blockers".Current Cardiovascular Drugs.Current Science Group.ISBN978-1-57340-221-7.RetrievedSeptember 7,2010.
  4. ^abcBarranger K, Vivian E, Peterson AM (2006)."Hypertension".In Arcangelo VP, Peterson AM (eds.).Pharmacotherapeutics for advanced practice: a practical approach.Lippincott Williams & Wilkins. p. 205.ISBN978-0-7817-5784-3.RetrievedSeptember 7,2010.
  5. ^Clément K, Vaisse C, Manning BS, Basdevant A, Guy-Grand B, Ruiz J, et al. (August 1995)."Genetic variation in the beta 3-adrenergic receptor and an increased capacity to gain weight in patients with morbid obesity".The New England Journal of Medicine.333(6): 352–354.doi:10.1056/NEJM199508103330605.PMID7609752.
  6. ^"Sir James Black, OM".The Telegraph.March 23, 2010.Archivedfrom the original on March 27, 2010.RetrievedMarch 25,2010.
  7. ^van der Vring JA, Daniëls MC, Holwerda NJ, Withagen PJ, Schelling A, Cleophas TJ, Hendriks MG (June 1999). "Combination of calcium channel blockers and beta blockers for patients with exercise-induced angina pectoris: a double-blind parallel-group comparison of different classes of calcium channel blockers. The Netherlands Working Group on Cardiovascular Research (WCN)".Angiology.50(6): 447–454.doi:10.1177/000331979905000602.PMID10378820.S2CID21885509.
  8. ^Stapleton MP (1997)."Sir James Black and propranolol. The role of the basic sciences in the history of cardiovascular pharmacology".Texas Heart Institute Journal.24(4): 336–342.PMC325477.PMID9456487.
  9. ^Wiysonge CS, Bradley HA, Volmink J, Mayosi BM, Opie LH (January 2017)."Beta-blockers for hypertension".The Cochrane Database of Systematic Reviews.1(1): CD002003.doi:10.1002/14651858.CD002003.pub5.PMC5369873.PMID28107561.
  10. ^Reinhart, Marcia; Puil, Lorri; Salzwedel, Douglas M.; Wright, James M. (July 13, 2023)."First-line diuretics versus other classes of antihypertensive drugs for hypertension".The Cochrane Database of Systematic Reviews.2023(7): CD008161.doi:10.1002/14651858.CD008161.pub3.ISSN1469-493X.PMC10339786.PMID37439548.
  11. ^Zhu J, Chen N, Zhou M, Guo J, Zhu C, Zhou J, et al. (January 2022)."Calcium channel blockers versus other classes of drugs for hypertension".The Cochrane Database of Systematic Reviews.1(1): CD003654.doi:10.1002/14651858.CD003654.pub6.PMC8742884.PMID35000192.
  12. ^Wiysonge CS, Bradley HA, Volmink J, Mayosi BM, Opie LH (January 2017)."Beta-blockers for hypertension".The Cochrane Database of Systematic Reviews.1(1): CD002003.doi:10.1002/14651858.cd002003.pub5.PMC5369873.PMID28107561.
  13. ^Opie LH (2009).Drugs for the Heart.Philadelphia: Saunders. pp. 6–18.ISBN978-1-4160-6158-8.
  14. ^Hjalmarson A, Goldstein S, Fagerberg B, Wedel H, Waagstein F, Kjekshus J, et al. (March 2000)."Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group".JAMA.283(10): 1295–1302.doi:10.1001/jama.283.10.1295.PMID10714728.
  15. ^Leizorovicz A, Lechat P, Cucherat M, Bugnard F (February 2002). "Bisoprolol for the treatment of chronic heart failure: a meta-analysis on individual data of two placebo-controlled studies—CIBIS and CIBIS II. Cardiac Insufficiency Bisoprolol Study".American Heart Journal.143(2): 301–307.doi:10.1067/mhj.2002.120768.PMID11835035.
  16. ^Packer M, Fowler MB, Roecker EB, Coats AJ, Katus HA, Krum H, et al. (October 2002)."Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival (COPERNICUS) study".Circulation.106(17): 2194–2199.doi:10.1161/01.CIR.0000035653.72855.BF.PMID12390947.
  17. ^Fletcher P (2000)."Beta blockers in heart failure".Australian Prescriber.23(6): 120–123.doi:10.18773/austprescr.2000.138.
  18. ^"Use of beta-blockers and ivabradine in heart failure with reduced ejection fraction".www.uptodate.com.Archivedfrom the original on December 22, 2015.RetrievedDecember 11,2015.
  19. ^Pritchett AM, Redfield MM (August 2002)."Beta-blockers: new standard therapy for heart failure".Mayo Clinic Proceedings.77(8): 839–845, quiz 845–46.doi:10.4065/77.8.839.PMID12173717.
  20. ^Alabed S, Sabouni A, Al Dakhoul S, Bdaiwi Y, et al. (Cochrane Heart Group) (July 2020)."Beta-blockers for congestive heart failure in children".The Cochrane Database of Systematic Reviews.2020(7): CD007037.doi:10.1002/14651858.CD007037.pub4.PMC7389334.PMID32700759.
  21. ^Goodman & Gilman's: The Pharmacological Basic of Therapeutics.McGraw-Hill. 2018.ISBN9781259584732.
  22. ^abcdeSafi S, Sethi NJ, Nielsen EE, Feinberg J, Jakobsen JC, Gluud C, et al. (Cochrane Heart Group) (December 2019)."Beta-blockers for suspected or diagnosed acute myocardial infarction".The Cochrane Database of Systematic Reviews.12(12): CD012484.doi:10.1002/14651858.CD012484.pub2.PMC6915833.PMID31845756.
  23. ^abFarzam K, Jan A (2023)."Beta Blockers".StatPearls.Treasure Island (FL): StatPearls Publishing.PMID30422501.RetrievedOctober 31,2023.
  24. ^Iqbal AH, Jamal SF (2023)."Essential Hypertension".StatPearls.Treasure Island (FL): StatPearls Publishing.PMID30969681.RetrievedOctober 31,2023.
  25. ^abWong GW, Wright JM, et al. (Cochrane Hypertension Group) (February 2014)."Blood pressure lowering efficacy of nonselective beta-blockers for primary hypertension".The Cochrane Database of Systematic Reviews.2014(2): CD007452.doi:10.1002/14651858.CD007452.pub2.PMC10603273.PMID24585007.
  26. ^abWiysonge CS, Bradley HA, Volmink J, Mayosi BM, Opie LH, et al. (Cochrane Hypertension Group) (January 2017)."Beta-blockers for hypertension".The Cochrane Database of Systematic Reviews.1(1): CD002003.doi:10.1002/14651858.CD002003.pub5.PMC5369873.PMID28107561..
  27. ^Schneier FR (September 2006). "Clinical practice. Social anxiety disorder".The New England Journal of Medicine.355(10): 1029–1036.doi:10.1056/NEJMcp060145.PMID16957148.
  28. ^Tyrer P (January 1992). "Anxiolytics not acting at the benzodiazepine receptor: beta blockers".Progress in Neuro-Psychopharmacology & Biological Psychiatry.16(1): 17–26.doi:10.1016/0278-5846(92)90004-X.PMID1348368.S2CID24742562.
  29. ^abTindall B (October 17, 2004)."Better Playing Through Chemistry".The New York Times.Archived fromthe originalon August 26, 2015.
  30. ^Blessberger H, Lewis SR, Pritchard MW, Fawcett LJ, Domanovits H, Schlager O, et al. (September 2019)."Perioperative beta-blockers for preventing surgery-related mortality and morbidity in adults undergoing cardiac surgery".The Cochrane Database of Systematic Reviews.9(9): CD013435.doi:10.1002/14651858.CD013435.PMC6755267.PMID31544227.
  31. ^abBlessberger H, Lewis SR, Pritchard MW, Fawcett LJ, Domanovits H, Schlager O, et al. (September 2019)."Perioperative beta-blockers for preventing surgery-related mortality and morbidity in adults undergoing non-cardiac surgery".The Cochrane Database of Systematic Reviews.2019(9): CD013438.doi:10.1002/14651858.CD013438.PMC6761481.PMID31556094.
  32. ^abChan KK, Lai P, Wright JM, et al. (Cochrane Hypertension Group) (February 2014)."First-line beta-blockers versus other antihypertensive medications for chronic type B aortic dissection".The Cochrane Database of Systematic Reviews.2014(2): CD010426.doi:10.1002/14651858.CD010426.pub2.PMC10726980.PMID24570114.
  33. ^Koo HK, Lawrence KA, Musini VM, et al. (Cochrane Heart Group) (November 2017)."Beta-blockers for preventing aortic dissection in Marfan syndrome".The Cochrane Database of Systematic Reviews.2017(11): CD011103.doi:10.1002/14651858.CD011103.pub2.PMC6486285.PMID29110304.
  34. ^abTim Glover."Golf: O'Grady says players use beta-blockers: Drugs 'helped win majors'".The Independent.Archivedfrom the original on September 25, 2015.RetrievedMarch 28,2017.
  35. ^World Anti-Doping Agency (September 19, 2005)."The World Anti-Doping Code: The 2006 Prohibited List International Standard"(PDF).World Anti-Doping Agency.Archived(PDF)from the original on February 11, 2017.RetrievedFebruary 10,2017.
  36. ^Scott M (August 15, 2008)."Olympics: North Korea's Kim Jong-su loses medals after positive drugs test".The Guardian.Guardian News and Media Limited.RetrievedMarch 7,2018.
  37. ^Elman MJ, Sugar J, Fiscella R, Deutsch TA, Noth J, Nyberg M, et al. (1998)."The effect of propranolol versus placebo on resident surgical performance".Transactions of the American Ophthalmological Society.96:283–91, discussion 291–4.PMC1298399.PMID10360293.
  38. ^"Musicians Use Beta Blockers as Performance-Enabling Drugs".WQXR. August 16, 2013.RetrievedMarch 11,2021.
  39. ^abcRossi S, ed. (2006).Australian Medicines Handbook.Adelaide: Australian Medicines Handbook.
  40. ^Cruickshank JM (2010). "Beta-blockers and heart failure".Indian Heart Journal.62(2): 101–110.PMID21180298.
  41. ^Beta-Adrenoceptor Antagonists (Beta-Blockers);"Beta-Adrenoceptor Antagonists (Beta-Blockers)".CV Pharmacology.Archivedfrom the original on August 8, 2011.RetrievedAugust 8,2011.
  42. ^Elliott WJ, Meyer PM (January 2007). "Incident diabetes in clinical trials of antihypertensive drugs: a network meta-analysis".Lancet.369(9557): 201–207.doi:10.1016/S0140-6736(07)60108-1.PMID17240286.S2CID37044384.
  43. ^Mayor S (July 2006)."NICE removes beta blockers as first line treatment for hypertension".BMJ.333(7557): 8.doi:10.1136/bmj.333.7557.8-a.PMC1488775.PMID16809680.
  44. ^Richards JR, Derlet RW, Albertson TE."Methamphetamine Toxicity: Treatment & Management".Medscape.WebMD.Archivedfrom the original on April 9, 2016.RetrievedApril 20,2016.
  45. ^abRichards JR, Albertson TE, Derlet RW, Lange RA, Olson KR, Horowitz BZ (May 2015). "Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review".Drug and Alcohol Dependence.150:1–13.doi:10.1016/j.drugalcdep.2015.01.040.PMID25724076.
  46. ^Handly M (December 16, 2016)."Toxicity, Amphetamine".Medscape.Archivedfrom the original on October 13, 2007.
  47. ^abcdefghiWyeth."Propranolol hydrochloride"(PDF).RetrievedSeptember 3,2020.
  48. ^National Heart, Lung, and Blood Institute(2007)."Expert Panel Report 3 (EPR-3): Guidelines for the Diagnosis and Management of Asthma–Summary Report 2007".The Journal of Allergy and Clinical Immunology.120(5): S94–S138.doi:10.1016/j.jaci.2007.09.029.Archived fromthe originalon August 28, 2021.RetrievedDecember 9,2017.
  49. ^abMorales DR, Jackson C, Lipworth BJ, Donnan PT, Guthrie B (April 2014). "Adverse respiratory effect of acute β-blocker exposure in asthma: a systematic review and meta-analysis of randomized controlled trials".Chest.145(4). Elsevier BV: 779–786.doi:10.1378/chest.13-1235.PMID24202435.
  50. ^Salpeter SR, Ormiston TM, Salpeter EE (November 2002)."Cardioselective beta-blockers in patients with reactive airway disease: a meta-analysis".Annals of Internal Medicine.137(9). American College of Physicians: 715–725.doi:10.7326/0003-4819-137-9-200211050-00035.PMID12416945.
  51. ^Sprague JE, Arbeláez AM (September 2011)."Glucose counterregulatory responses to hypoglycemia".Pediatric Endocrinology Reviews.9(1): 463–475.PMC3755377.PMID22783644.
  52. ^Weinstein RS, Cole S, Knaster HB, Dahlbert T (February 1985). "Beta blocker overdose with propranolol and with atenolol".Annals of Emergency Medicine.14(2): 161–163.doi:10.1016/S0196-0644(85)81081-7.PMID2857542.
  53. ^"Toxicity, Beta-blocker: Treatment & Medication – eMedicine Emergency Medicine".Archivedfrom the original on March 17, 2009.RetrievedMarch 6,2009.
  54. ^John Gualtier."Beta-Adrenergic Blocker Poisoning"(PDF).Courses.ahc.umn.edu.Archived fromthe original(PDF)on March 3, 2016.RetrievedMarch 28,2017.
  55. ^USMLE WORLD 2009 Step1, Pharmacology, Q85
  56. ^Michel MC, Insel PA (2006)."Adrenergic Receptors in Clinical Medicine".In Perez DM (ed.).The Adrenergic Receptors in the 21st Century.Humana Press. p. 135.ISBN978-1-58829-423-4.RetrievedSeptember 8,2010.[permanent dead link]
  57. ^Jameson JL, Loscalzo J (2010).Harrison's Nephrology and Acid-Base Disorders.McGraw-Hill Companies. p. 215.ISBN978-0-07-166339-7.RetrievedSeptember 8,2010.
  58. ^Lewis KP, Gonzalez RM, Balonov K (2009)."Vasoactive Amines and Inotropic Agents".In O'Donnell JM, Nácul FE (eds.).Surgical Intensive Care Medicine.Springer. p. 47.ISBN978-0-387-77892-1.RetrievedSeptember 8,2010.
  59. ^Ahrens RC (1990). "Skeletal muscle tremor and the influence of adrenergic drugs".The Journal of Asthma.27(1): 11–20.doi:10.3109/02770909009073289.PMID1968452.
  60. ^Reents S (2000).Sport and exercise pharmacology.Human Kinetics. p. 19.ISBN978-0-87322-937-1.RetrievedSeptember 10,2010.
  61. ^Martini FH (2005).Anatomy and Physiology.Pearson Education. p. 394.ISBN978-0-8053-5947-3.RetrievedSeptember 10,2010.
  62. ^Khan MI (2006)."Beta-Blockers".Encyclopedia of Heart Diseases.Elsevier. p. 160.ISBN978-0-12-406061-6.RetrievedSeptember 10,2010.
  63. ^Lamster IB,Northridge ME,eds. (2008).Improving Oral Health for the Elderly: An Interdisciplinary Approach.New York: Springer. p. 87.ISBN978-0-387-74337-0.RetrievedOctober 23,2010.
  64. ^Rothfeld GS, Romaine DS (2005)."Beta Antagonist (Blocker) Medications".The Encyclopedia of Men's Health.Amaranth. p. 48.ISBN978-0-8160-5177-9.RetrievedOctober 23,2010.
  65. ^Manger WM, Gifford RW (2001).100 Questions and Answers about Hypertension.Blackwell Science. p.106.ISBN978-0-632-04481-8.RetrievedSeptember 10,2010.beta blockers dilation of blood vessels.
  66. ^Hurst J (1997)."Hypertension: Epidemiology, Pathophysiology, Diagnosis and Treatment".In Schlant RC (ed.).Hurst's the Heart.Vol. 2. Blackwell Science. p. 1564.ISBN978-0-07-912951-2.RetrievedOctober 7,2010.
  67. ^Reid JL (2001).Lecture notes on clinical pharmacology.Vol. 6. Blackwell Science. p. 76.ISBN978-0-632-05077-2.RetrievedMarch 11,2011.
  68. ^"Labetalol Hydrochloride Monograph for Professionals".Drugs.com.American Society of Health-System Pharmacists.RetrievedMarch 3,2019.
  69. ^"Coreg - Food and Drug Administration"(PDF).
  70. ^abcdefghCojocariu SA, Maștaleru A, Sascău RA, Stătescu C, Mitu F, Leon-Constantin MM (February 2021)."Neuropsychiatric Consequences of Lipophilic Beta-Blockers".Medicina.57(2): 155.doi:10.3390/medicina57020155.PMC7914867.PMID33572109.
  71. ^Stoschitzky, K.; Sakotnik, A.; Lercher, P.; Zweiker, R.; Maier, R.; Liebmann, P.; Lindner, W. (April 1999)."Influence of beta-blockers on melatonin release".European Journal of Clinical Pharmacology.55(2): 111–115.doi:10.1007/s002280050604.ISSN0031-6970.PMID10335905.S2CID32317760.
  72. ^Tikhomirova, O. V.; Zybina, N. N.; Kozhevnikova, V. V. (May 1, 2022)."Effects of Prolonged Use of β-Adrenoblockers on Melatonin Secretion, Sleep Quality, and Vascular Brain Damage".Neuroscience and Behavioral Physiology.52(4): 500–504.doi:10.1007/s11055-022-01270-y.ISSN1573-899X.S2CID250708105.
  73. ^Gehrman, Philip R.; Anafi, Ron C. (October 2021)."Treatment of a patient with a circadian sleep-wake disorder using a combination of melatonin and metoprolol".Journal of Clinical Sleep Medicine.17(10): 2121–2124.doi:10.5664/jcsm.9410.ISSN1550-9389.PMC8494102.PMID34032203.
  74. ^abcdefghijklmnopqrst"Comparison of Oral Beta-Blockers".pharmacist.therapeuticresearch.com.Therapeutic Research Center.Archivedfrom the original on October 18, 2017.RetrievedApril 30,2017.
  75. ^Rosendorff C (June 1993). "Beta-blocking agents with vasodilator activity".Journal of Hypertension Supplement.11(4): S37–S40.doi:10.1097/00004872-199306003-00009.PMID8104240.
  76. ^"CARTEOLOL".pubchem.ncbi.nlm.nih.gov.U.S. National Library of Medicine.Archivedfrom the original on October 18, 2017.RetrievedOctober 18,2017.
  77. ^ab"oxprenolol".pubchem.ncbi.nlm.nih.gov.U.S. National Library of Medicine.Archivedfrom the original on October 18, 2017.RetrievedOctober 18,2017.
  78. ^ab"Celiprolol".pubchem.ncbi.nlm.nih.gov.U.S. National Library of Medicine.Archivedfrom the original on October 18, 2017.RetrievedOctober 18,2017.
  79. ^Volz-Zang C, Eckrich B, Jahn P, Schneidrowski B, Schulte B, Palm D (1994). "Esmolol, an ultrashort-acting, selective beta 1-adrenoceptor antagonist: pharmacodynamic and pharmacokinetic properties".European Journal of Clinical Pharmacology.46(5): 399–404.doi:10.1007/BF00191900.PMID7957532.S2CID12809602.
  80. ^Sinha SS, Gurm HS (February 2014)."The double jeopardy of chronic obstructive pulmonary disease and myocardial infarction".Open Heart.1(1): e000010.doi:10.1136/openhrt-2013-000010.PMC4189253.PMID25332777.
  81. ^"Butaxamine".pubchem.ncbi.nlm.nih.gov.U.S. National Library of Medicine.Archivedfrom the original on October 18, 2017.RetrievedOctober 18,2017.
  82. ^"ICI 118551".ChEBI.
  83. ^"SR 59230A".pubchem.ncbi.nlm.nih.gov.U.S. National Library of Medicine.Archivedfrom the original on October 18, 2017.RetrievedOctober 18,2017.
  84. ^abcLarochelle P, Tobe SW, Lacourcière Y (May 2014)."β-Blockers in hypertension: studies and meta-analyses over the years".The Canadian Journal of Cardiology.30(5 Suppl): S16–S22.doi:10.1016/j.cjca.2014.02.012.PMID24750978.
  85. ^Ganten D, Mulrow PJ, eds. (1990).Pharmacology of Antihypertensive Therapeutics.Berlin, Heidelberg: Springer Berlin Heidelberg. p. 523.ISBN9783642742095.
  86. ^Zipursky JS, Macdonald EM, Luo J, Gomes T, Mamdani MM, Paterson JM, Juurlink DN (June 2017). "Lipophilic β-Blockers and Suicide in the Elderly".Journal of Clinical Psychopharmacology.37(3): 381–384.doi:10.1097/JCP.0000000000000695.PMID28338548.S2CID23355130.
  87. ^abcdeAronson JK (June 2008)."Changing beta-blockers in heart failure: when is a class not a class?".The British Journal of General Practice.58(551): 387–389.doi:10.3399/bjgp08X299317.PMC2418988.PMID18505613.
  88. ^"DailyMed - BREVIBLOC- esmolol hydrochloride injection".DailyMed.U.S. National Library of Medicine.RetrievedNovember 9,2022.
  89. ^"DailyMed - BETAPACE- sotalol hydrochloride tablet BETAPACE AF- sotalol hydrochloride tablet".DailyMed.U.S. National Library of Medicine.RetrievedNovember 9,2022.
  90. ^"Announcement of Approval of Additional Indications for Onoact 50 for Injection, Short-Acting Selective ß1 Blocker".www.evaluategroup.com.Evaluate Ltd.RetrievedOctober 18,2017.
  91. ^"Metiprapanol – metipranolol solution/ drops".DailyMed.U.S. National Library of Medicine – NIH.Archivedfrom the original on October 18, 2017.RetrievedOctober 18,2017.
  92. ^"Drugs to Prevent Migraine in Adults".pharmacist.therapeuticresearch.com.Therapeutic Research Center.Archivedfrom the original on October 18, 2017.RetrievedApril 30,2017.
  93. ^Fares A (July 2011)."Night-time exogenous melatonin administration may be a beneficial treatment for sleeping disorders in beta blocker patients".Journal of Cardiovascular Disease Research.2(3): 153–155.doi:10.4103/0975-3583.85261.PMC3195193.PMID22022142.
  94. ^Choy C, Raytis JL, Smith DD, Duenas M, Neman J, Jandial R, Lew MW (June 2016)."Inhibition of β2-adrenergic receptor reduces triple-negative breast cancer brain metastases: The potential benefit of perioperative β-blockade".Oncology Reports.35(6): 3135–3142.doi:10.3892/or.2016.4710.PMC4869944.PMID27035124.
  95. ^Kokolus KM, Zhang Y, Sivik JM, Schmeck C, Zhu J, Repasky EA, et al. (2018)."Beta blocker use correlates with better overall survival in metastatic melanoma patients and improves the efficacy of immunotherapies in mice".Oncoimmunology.7(3): e1405205.doi:10.1080/2162402X.2017.1405205.PMC5790362.PMID29399407.
  96. ^Livingstone E, Hollestein LM, van Herk-Sukel MP, van de Poll-Franse L, Nijsten T, Schadendorf D, de Vries E (December 2013). "β-Blocker use and all-cause mortality of melanoma patients: results from a population-based Dutch cohort study".European Journal of Cancer.49(18): 3863–3871.doi:10.1016/j.ejca.2013.07.141.PMID23942335.
  97. ^Cardwell CR, Coleman HG, Murray LJ, O'Sullivan JM, Powe DG (June 2014). "Beta-blocker usage and prostate cancer survival: a nested case-control study in the UK Clinical Practice Research Datalink cohort".Cancer Epidemiology.38(3): 279–285.doi:10.1016/j.canep.2014.03.011.PMID24786858.
  98. ^Kim HY, Jung YJ, Lee SH, Jung HJ, Pak K (2017). "Is Beta-Blocker Use Beneficial in Breast Cancer? A Meta-Analysis".Oncology.92(5): 264–268.doi:10.1159/000455143.PMID28132057.S2CID5463335.
  99. ^Joseph S (1997). "Chapter 3, Schizoid Personality Disorder.".Personality Disorders: New Symptom-Focused Drug Therapy.Psychology Press. pp. 45–56.ISBN9780789001344.
  100. ^Cheine, M.; Ahonen, J.; Wahlbeck, K. (2001)."Beta-blocker supplementation of standard drug treatment for schizophrenia".The Cochrane Database of Systematic Reviews(3): CD000234.doi:10.1002/14651858.CD000234.ISSN1469-493X.PMID11686955.
  101. ^Shek E, Bardhan S, Cheine MV, Ahonen J, Wahlbeck, et al. (Cochrane Schizophrenia Group) (September 1996)."Beta-blocker supplementation of standard drug treatment for schizophrenia".Cochrane Database of Systematic Reviews.2010(7).doi:10.1002/14651858.CD000234.S2CID1627733.
  102. ^Boehm I, Morelli J, Nairz K, Silva Hasembank Keller P, Heverhagen JT (November 2016). "Beta blockers and intravenous roentgen contrast materials: Which risks do exist?".European Journal of Internal Medicine.35:e17–e18.doi:10.1016/j.ejim.2016.08.003.PMID27531627.
[edit]
Retrieved from "https://en.wikipedia.org/w/index.php?title=Beta_blocker&oldid=1234614046"