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20-September-2008 09:55:47 - blocker Skeletal formula of propranolol, the first clinically successful beta blocker Skeletal formula of propranolol, the first clinically successful beta blocker Beta blockers sometimes written as β-blocker are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias and cardioprotection after myocardial infarction heart attack. While once first-line treatment for hypertension, their role was downgraded in June 2006 in the United Kingdom to fourth-line as they did not perform as well as other drugs, particularly in the elderly, and there is increasing evidence that the most frequently used beta-blockers especially in combination with thiazide-type diuretics carry an unacceptable risk of provoking type 2 diabetes.1 However, Forest Laboratories and Mylan Inc. announced on December 18, 2007 the novel beta blocker Bystolic was approved by the FDA for treatment of hypertension. Propranolol was the first clinically useful beta adrenergic receptor antagonist. Invented by Sir James W. Black, it revolutionized the medical management of angina pectoris and is considered to be one of the most important contributions to clinical medicine and pharmacology of the 20th century.2 Beta blockers may also be referred to as beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists. The bureaucratic delays in allowing beta blockers to be brought to market are cited by libertarians as reasons for eliminating the need for FDA approval of new drugs. Goldberg notes, The FDA held up approval of beta blockers for eight years because it believed they caused cancer. In the meantime, according to Dr. Louis Lasagna of the Tufts University Center for the Study of Drug Development, 119,000 people died who might have been helped by that medication.3 Contents 1 Pharmacology 1.1 β-Receptor antagonism 1.2 Intrinsic sympathomimetic activity 1.3 α1-Receptor antagonism 1.4 Other effects 2 Clinical use 2.1 Congestive heart failure 2.2 Anxiety and performance enhancement 3 Adverse effects 4 Examples of beta blockers 4.1 Non-selective agents 4.2 β1-Selective agents 4.3 Mixed α1/β-adrenergic antagonists 4.4 β2-Selective agents 5 Side Effects / Health Consequences 6 Comparative information 6.1 Pharmacological differences 6.2 Indication differences 7 Footnotes 8 External links Pharmacology Beta blockers block the action of endogenous catecholamines epinephrine adrenaline and norepinephrine noradrenaline in particular, on β-adrenergic receptors, part of the sympathetic nervous system which mediates the fight or flight response. There are three known types of beta receptor, designated β1, β2 and β3. β1-Adrenergic receptors are located mainly in the heart and in the kidneys. β2-Adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. β3-receptors are located in fat cells. Examples of beta-blockers include: Sectral acebutolol, Zebeta bisoprolol, Brevibloc esmolol, Inderal propranolol, Tenormin atenolol, Normodyne labetalol, Coreg carvedilol, Lopressor metoprolol, and Bystolic nebivolol. β-Receptor antagonism Stimulation of β1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β1 receptors on the kidney causes renin release. Stimulation of β2 receptors induces smooth muscle relaxation resulting in vasodilation and bronchodilation amongst other actions, induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle. Stimulation of β3 receptors induces lipolysis. Beta blockers inhibit these normal epinephrine-mediated sympathetic actions, but have minimal effect on resting subjects. That is, they reduce the effect of excitement/physical exertion on heart rate and force of contraction, dilation of blood vessels and opening of bronchi, and also reduce tremor and breakdown of glycogen. It is therefore expected that non-selective beta blockers have an antihypertensive effect. The antihypertensive mechanism appears to involve: reduction in cardiac output due to negative chronotropic and inotropic effects, reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity for those β-blockers that do cross the blood-brain barrier, e.g. Propranolol. Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand. The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade - resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade. Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via the renin angiotensin aldosterone system with a resultant decrease in blood pressure due to decreased sodium and water retention. Intrinsic sympathomimetic activity Some beta blockers e.g. oxprenolol, pindolol, penbutolol and acebutolol exhibit intrinsic sympathomimetic activity ISA. These agents are capable of exerting low level agonist activity at the β-adrenergic receptor while simultaneously acting as a receptor site antagonist. These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy. Agents with ISA are not used in post-myocardial infarction as they have not been demonstrated to be beneficial. They may also be less effective than other beta blockers in the management of angina and tachyarrhythmia.4 α1-Receptor antagonism Some beta blockers e.g. labetalol and carvedilol exhibit mixed antagonism of both β- and α1-adrenergic receptors, which provides additional arteriolar vasodilating action. Other effects Beta blockers decrease nocturnal melatonin release, perhaps partly accounting for sleep disturbance caused by some agents.5 Beta blockers protect against social anxiety: Improvement of physical symptoms has been demonstrated with beta-blockers such as propranolol; however, these effects are limited to the social anxiety experienced in performance situations. example- an inexperienced symphony soloist 6 Beta blockers can impair the relaxation of bronchial muscle mediated by beta-2 and so should be avoided by asthmatics. They can also be used to treat glaucoma because they decrease intraocular pressure by lowering aqueous humor secretion.7 Clinical use Large differences exist in the pharmacology of agents within the class, thus not all beta blockers are used for all indications listed below. Indications for beta blockers include: Hypertension Angina Mitral valve prolapse Cardiac arrhythmia Congestive heart failure Myocardial infarction Glaucoma Migraine prophylaxis Symptomatic control tachycardia, tremor in anxiety and hyperthyroidism Essential tremor Phaeochromocytoma, in conjunction with α-blocker Beta blockers have also been used in the following conditions: Hypertrophic obstructive cardiomyopathy Acute dissecting aortic aneurysm Marfan syndrome chronic treatment with propranolol slows progression of aortic dilation and its complications Prevention of variceal bleeding in portal hypertension Possible mitigation of hyperhidrosis Social anxiety disorder and other anxiety disorders Congestive heart failure Although beta blockers were once contraindicated in congestive heart failure, as they have the potential to worsen the condition, studies in the late 1990s showed their positive effects on morbidity and mortality in congestive heart failure.8 9 10 Bisoprolol, carvedilol and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in congestive heart failure. Beta blockers are primarily known for their reductive effect on heart rate, although this is not necessarily the case. Beta blockers don't directly interact with the heart at all, but instead influence the renin/ angiotensin system at the kidneys. Beta blockers specifically cause a decrease in renin secretion, which in turn reduce the heart oxygen demand by lowering extracellular volume. Beta blockers have also been a benefit to improving the ejection fraction of the heart despite an initial reduction in it. Trials have shown that Beta blockers reduce the absolute risk of death by 4.5% over a 13 month period. As well as reducing the risk of mortality, the number of hospital visits and hospitalizations were also reduced in the trials.11 Anxiety and performance enhancement Some people, particularly musicians, use beta blockers to avoid stage fright and tremor during public performance and auditions. The physiological symptoms of the fight/flight response associated with performance anxiety and panic pounding heart, cold/clammy hands, increased respiration, sweating, etc. are significantly reduced, thus enabling anxious individuals to concentrate on the task at hand. Officially, beta blockers are not approved for anxiolytic use by the U.S. Food and Drug Administration. 12 Since they lower heart rate and reduce tremor, beta blockers have been used by some Olympic marksmen to enhance performance, though beta blockers are banned by the International Olympic Committee IOC.13 Although they have no recognisable benefit to most sports, it is acknowledged that they are beneficial to sports such as archery and shooting. A recent, high-profile transgression taking place in the 2008 Beijing Olympic Games, where 50m Pistol silver medallist, and 10m Air-pistol bronze medallist Kim Jong-su tested positive for the Beta-blocker, Propranolol. Adverse effects Adverse drug reactions ADRs associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, abnormal vision, decreased concentration, hallucinations, insomnia, nightmares, clinical depression, sexual dysfunction, erectile dysfunction and/or alteration of glucose and lipid metabolism. Mixed α1/β-antagonist therapy is also commonly associated with orthostatic hypotension. Carvedilol therapy is commonly associated with edema.4 Central nervous system CNS adverse effects hallucinations, insomnia, nightmares, depression are more common in agents with greater lipid solubility, which are able to cross the blood-brain barrier into the CNS. Similarly, CNS adverse effects are less common in agents with greater aqueous solubility listed below. 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, however receptor selectivity diminishes at higher doses. Beta blockade, especially of the beta-1 receptor at the macula densa inhibits renin release, thus decreasing the release of aldosterone. This causes hyponatremia and hyperkalemia. A 2007 study revealed that diuretics and beta-blockers used for hypertension increase a patient's risk of developing diabetes while ACE inhibitors and Angiotensin II receptor antagonists Angiotensin Receptor Blockers actually decrease the risk of diabetes.14 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.15 Beta blockers must not be used in the treatment of cocaine, amphetamine, or other alpha adrenergic stimulant overdose. The blockade of only beta receptors increases hypertension, reduces coronary blood flow, left ventricular function, and cardiac output and tissue perfusion by means of leaving the alpha adrenergic system stimulation unopposed. 16 The appropriate antihypertensive drugs to administer during hypertensive crisis resulting from stimulant abuse are vasodilators like nitroglycerin, diuretics like furosemide and alpha blockers like phentolamine. 17 Examples of beta blockers Dichloroisoprenaline, the first beta blocker. Dichloroisoprenaline, the first beta blocker. Non-selective agents Alprenolol Carteolol Levobunolol Mepindolol Metipranolol Nadolol Oxprenolol Penbutolol Pindolol Propranolol Sotalol Timolol β1-Selective agents Acebutolol Atenolol Betaxolol Bisoprolol18 Esmolol Metoprolol Nebivolol Amosulalol Landiolol Tilisolol Mixed α1/β-adrenergic antagonists Arotinolol Carvedilol Celiprolol Labetalol β2-Selective agents Butaxamine weak α-adrenergic agonist activity Side Effects / Health Consequences Low Blood Pressure Slow Heart Rate Impaired Circulation Loss of Sleep Heart Failure Asthma Depression Sexual Dysfunction Nausea Headaches Dizziness Muscle Cramps Peyronie's disease Comparative information Pharmacological differences Agents with intrinsic sympathomimetic action ISA Acebutolol, carteolol, celiprolol, mepindolol, oxprenolol, pindolol Agents with greater aqueous solubility Atenolol, celiprolol, nadolol, sotalol Agents with membrane stabilising activity Acebutolol, betaxolol, pindolol, propranolol Agents with antioxidant effect Carvedilol Nebivolol Indication differences Agents specifically indicated for cardiac arrhythmia Esmolol, sotalol, landiolol Agents specifically indicated for congestive heart failure Bisoprolol, carvedilol, sustained-release metoprolol, nebivolol Agents specifically indicated for glaucoma Betaxolol, carteolol, levobunolol, metipranolol, timolol Agents specifically indicated for myocardial infarction Atenolol, metoprolol, propranolol Agents specifically indicated for migraine prophylaxis Timolol, propranolol Propranolol is the only agent indicated for control of tremor, portal hypertension and esophageal variceal bleeding, and used in conjunction with α-blocker therapy in phaeochromocytoma.4 Footnotes ^ Sheetal Ladva 2006-06-28. NICE and BHS launch updated hypertension guideline. National Institute for Health and Clinical Excellence. Retrieved on 2006-09-30. ^ Melanie Patricia Stapleton 1997. Sir James Black and Propranolol. Texas Heart Institute Journal. ^ http://www.cato.org/pubs/regulation/reg18n2c.html ^ a b c 2006 in or Rossi S: Australian Medicines Handbook. Adelaide: Australian Medicines Handbook. ^ Stoschitzky K, Sakotnik A, Lercher P, et al 1999. Influence of beta-blockers on melatonin release. Eur. J. Clin. Pharmacol. 55 2: 111-5. doi:10.1007/s002280050604. PMID 10335905. ^ Davidson, M.D., Jonathan; Connor M.D., Kathryn M. 1999. Social Anxiety Disorder: A Treatable Condition. Drug Benefit Trends 115 5BH-7BH. Cliggott Publishing, Division of SCP Communications. Retrieved on 2007-10-06. ^ Shen, Howard 2008. Illustrated Pharmacology Memory Cards: PharMnemonics. Minireview, 15. ISBN 1-59541-101-1. ^ Hjalmarson A, Goldstein S, Fagerberg B, et al 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: 1295-302. doi:10.1001/jama.283.10.1295. PMID 10714728. ^ Leizorovicz A, Lechat P, Cucherat M, Bugnard F 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. Am. Heart J. 143 2: 301-7. doi:10.1067/mhj.2002.120768. PMID 11835035. ^ Packer M, Fowler MB, Roecker EB, et al 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: 2194-9. doi:10.1161/01.CIR.0000035653.72855.BF. PMID 12390947. ^ Pritchett AM, Redfield MM 2002. Beta-blockers: new standard therapy for heart failure PDF. Mayo Clin. Proc. 77 8: 839-45; quiz 845-6. PMID 12173717. ^ Schneier FR 2006. Clinical practice. Social anxiety disorder. N. Engl. J. Med. 355 10: 1029-36. doi:10.1056/NEJMcp060145. PMID 16957148. ^ World Anti-Doping Agency 2005-09-19. The World Anti-Doping Code: The 2006 Prohibited List International Standard. World Anti-Doping Agency. Retrieved on 2006-12-13. ^ Elliott WJ, Meyer PM 2007. Incident diabetes in clinical trials of antihypertensive drugs: a network meta-analysis. Lancet 369 9557: 201-7. doi:10.1016/S0140-67360760108-1. PMID 17240286. ^ Mayor S 2006. NICE removes beta blockers as first line treatment for hypertension. BMJ 333 7557: 8. doi:10.1136/bmj.333.7557.8-a. PMID 16809680. ^ eMedicine - Toxicity, Cocaine : Article by Carlos J Roldan ^ eMedicine - Toxicity, Amphetamine : Article by Neal Handly ^ Bisoprolol MedlinePlus External links Better Playing Through Chemistry by Blair Tindall, New York Times, October 17, 2004. Discusses the use of beta blockers among professional musicians Musicians using beta blockers by Blair Tindall. Condensed version of above article. In Defense of the Beta Blocker by Carl Elliott, The Atlantic, August 20, 2008. Discusses the use of propranolol by a North Korean pistol shooter in the 2008 Olympics MeSH beta-Adrenergic+Blockers v d e Adrenergic antagonists α α1 selective Doxazosin · Prazosin · Alfuzosin · Terazosin · Indoramin · Urapidil · Trimazosin · Moxisylyte · 1A Tamsulosin, Silodosin α2 selective Atipamezole · Efaroxan · Idazoxan · Yohimbine · Benzylpiperazine · Rauwolscine · Mirtazapine Non-selective α reversible Phentolamine · irreversible Phenoxybenzamine β β1 selective cardioselective Atenolol · Acebutolol · Celiprolol · Betaxolol · Bisoprolol · Esmolol · Metoprolol · Nebivolol β2 selective Butaxamine · ICI 118551 β3 selective SR 59230A Non-selective β Alprenolol · Amosulalol · Metipranolol · Nadolol · Oxprenolol · Penbutolol · Pindolol · Propranolol · Tertatolol · Timolol · Tilisolol · Sotalol Mixed α1/β Carvedilol · Labetalol · Arotinolol v d e Ophthalmologicals: antiglaucoma preparations and miotics S01E Sympathomimetics Apraclonidine Brimonidine Clonidine Dipivefrine Epinephrine Parasympathomimetics M: Aceclidine Pilocarpine M/N: Acetylcholine Carbachol AI: Demecarium Echothiophate Stigmine Fluostigmine, Neostigmine, Physostigmine Paraoxon Carbonic anhydrase inhibitors Acetazolamide Brinzolamide Diclofenamide Dorzolamide Methazolamide Beta blocking agents Befunolol Betaxolol Carteolol Levobunolol Metipranolol Timolol Prostaglandin analogues Bimatoprost Latanoprost Travoprost Unoprostone Other agents Dapiprazole Guanethidine v d e Major drug groups Gastrointestinal tract/metabolism A stomach acid Antacids, H2 antagonists, Proton pump inhibitors Antiemetics Laxatives Antidiarrhoeals/Antipropulsives Anti-obesity drugs Anti-diabetics Vitamins Dietary minerals Blood and blood forming organs B Antithrombotics Anticoagulants, Antiplatelets, Thrombolytics Antihemorrhagics Cardiovascular system C cardiac therapy/antianginals Cardiac glycosides, Antiarrhythmics, Cardiac stimulant Antihypertensives Diuretics Vasodilators Beta blockers renin-angiotensin system ACE inhibitors, Angiotensin II receptor antagonists, Renin inhibitors Antihyperlipidemics Skin D Emollients Cicatrizant Antipruritics Reproductive system G Hormonal contraception Fertility agents SERMs Sex hormones Endocrine system H Corticosteroids Sex hormones Thyroid hormones Antithyroid agent Infections and infestations J, P Antibiotics Antivirals Vaccines Antifungals Antiparasitic Antiprotozoals, Anthelmintics Malignant and immune disease L Anticancer agents Immunostimulators Immunosuppressants Muscles, bones, and joints M Anabolic steroids Anti-inflammatories NSAID Antirheumatics Corticosteroids Muscle relaxants Brain and nervous system N Anesthetics General, Local Analgesics Anticonvulsants Mood stabilizers Psycholeptic Anxiolytics, Antipsychotics, Hypnotics/Sedatives Psychoanaleptic Antidepressants, Stimulants/Psychostimulants Respiratory system R Bronchodilators Decongestants H1 antagonists Other ATC V Antidotes Contrast media Radiopharmaceuticals Dressing v d e Receptor agonists, antagonists, and reuptake inhibitors BA/M 5-HT serotonin receptor Serotonin receptor agonist 5-HT4 Serotonin antagonist 5-HT3 Serotonin uptake inhibitor SSRI Dopamine receptor Dopamine agonist Dopamine antagonist Dopamine reuptake inhibitor Adrenergic receptor Adrenergic agonist Alpha, Beta 1/2 Adrenergic antagonist Alpha 1/2, Beta Adrenergic uptake inhibitor Histamine receptor Histamine agonist Histamine antagonist H1, H2, H3 AA GABA receptor GABA agonist GABA antagonist Glutamate receptor NMDA receptor NMDA receptor antagonist AMPA receptor Ampakine Excitatory amino acid agonist Excitatory amino acid antagonist ANS Acetylcholine receptor Cholinergic Muscarinic, Nicotinic Anticholinergic Muscarinic, Nicotinic/Ganglionic blocker/Neuromuscular-blocking drugs Acetylcholinesterase inhibitor Adrenergic receptor SANS only -- see above for details PANS Parasympathomimetic Cholinergic, Acetylcholinesterase inhibitor - Parasympatholytic Anticholinergic, Ganglionic blocker SANS Sympathomimetic Adrenergic agonist, Monoamine oxidase inhibitor - Sympatholytic Adrenergic antagonist, Alpha blocker, Ganglionic blocker Retrieved from http://en..org/wiki/Beta_blocker Categories: Beta blockers | Antihypertensive agents Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages العربية Deutsch Español Ù?ارسی Français Hrvatski Italiano Nederlands 日本語 ‪Norsk bokmÃ¥l‬ Polski Português Suomi Svenska ไทย УкраїнÑ?ька This page was last modified on 20 August 2008, at 21:57
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