- 関
- p adrenergic receptor antagonist(s)
WordNet
- to remain unmolested, undisturbed, or uninterrupted -- used only in infinitive form; "let her be"
- work in a specific place, with a specific subject, or in a specific function; "He is a herpetologist"; "She is our resident philosopher" (同)follow
- have life, be alive; "Our great leader is no more"; "My grandfather lived until the end of war" (同)live
- be identical to; be someone or something; "The president of the company is John Smith"; "This is my house"
- happen, occur, take place; "I lost my wallet; this was during the visit to my parents house"; "There were two hundred people at his funeral"; "There was a lot of noise in the kitchen"
- have the quality of being; (copula, used with an adjective or a predicate noun); "John is rich"; "This is not a good answer"
- occupy a certain position or area; be somewhere; "Where is my umbrella?" "The toolshed is in the back"; "What is behind this behavior?"
- spend or use time; "I may be an hour"
- stake on the outcome of an issue; "I bet $100 on that new horse"; "She played all her money on the dark horse" (同)wager, play
- the act of gambling; "he did it on a bet" (同)wager
- maintain with or as if with a bet; "I bet she will be there!" (同)wager
- second in order of importance; "the candidate, considered a beta male, was perceived to be unable to lead his party to victory"
- the 2nd letter of the Greek alphabet
- preliminary or testing stage of a software or hardware product; "a beta version"; "beta software"
- a class of drugs that inhibit (block) some biological process (同)blocking_agent
- a football player whose responsibility is to block players attempting to stop an offensive play
- beets (同)genus Beta
PrepTutorEJDIC
- 《連結語として補語を伴なって…『である』,…だ,…です / 《位置・場所を表す語句を伴って》(…に)『ある』,いる(occupy a place or situation) / 〈物事が〉『存在する』,ある(exist);〈生物が〉生存する,生きている(live) / 行われる,起こる,発生する(take place, occur) / 存続する,そのままでいる(remain as before) / 《『be to』 do》 / …する予定である,…することになっている / …すべきだ / 《受動態の不定詞を伴って》…できる / 《命令》…するのだ / 《条件節に》…する意図がある / 《『if…were to』 do》…するとしたなら / 《『be』 do『ing』》《進行形》 / 《進行中の動作》…している,しつつある / 《近い未来》…しようとしている,するつもり / 《動作の反復》(いつも)…している / 《『be』+『他動詞の過去分詞』》《受動態》…される,されている / 《『be』+『自動詞の過去分詞』》《完了形》…した[状態にある]
- 『かけ』・(…との)かけ《+『with』+『名』》 / かけた物(金) / かけの対象 / 〈金・物〉'を'『かける』 / (かけ事・ゲームなどで)〈人〉‘と'『かけをする』《+『名』〈人〉+『on』+『名』》 / (…に)『かける』《+『on』(『against』)+『名』(one's do『ing』)》
- ベータ(ギリシア語アルファベットの第2文字;B,β;英語のB,b に遭当)
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/08/20 13:00:26」(JST)
wiki en
| Beta blockers β-blockers |
|
|---|---|
| Drug class | |
|
Skeletal formula of propranolol, the first clinically successful beta blocker
|
|
| Use | Hypertension, arrhythmia, etc. |
| Biological target | beta receptors |
| ATC code | C07 |
| External links | |
| MeSH | D000319 |
| AHFS/Drugs.com | Drug Classes |
| Consumer Reports | Best Buy Drugs |
| WebMD | medicinenet rxlist |
Beta blockers (β-blockers, beta-adrenergic blocking agents, beta antagonists, beta-adrenergic antagonists, beta-adrenoreceptor antagonists, or beta adrenergic receptor antagonists) are a class of drugs that target the beta receptor. Beta receptors are found on cells of the heart muscles, smooth muscles, airways, arteries, kidneys, and other tissues that are part of the sympathetic nervous system and lead to stress responses, especially when they are stimulated by epinephrine (adrenaline). Beta blockers interfere with the binding to the receptor of epinephrine and other stress hormones, and weaken the effects of stress hormones.
They are particularly used for the management of cardiac arrhythmias, protecting the heart from a second heart attack (myocardial infarction) after a first heart attack (secondary prevention),[1] and hypertension.[2]
In 1962, Sir James W. Black [3] found the first clinically significant beta blockers—propranolol and pronethalol; it revolutionized the medical management of angina pectoris[4] and is considered by many to be one of the most important contributions to clinical medicine and pharmacology of the 20th century.[5]
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.[6][7] Three types of beta receptors are known, designated β1, β2 and β3 receptors.[8] β1-adrenergic receptors are located mainly in the heart and in the kidneys.[7] β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.[7] β3-adrenergic receptors are located in fat cells.[9]
Contents
- 1 Medical uses
- 1.1 Congestive heart failure
- 1.2 Anxiety and performance enhancement
- 2 Adverse effects
- 2.1 Contraindications
- 2.2 Toxicity
- 3 β-Receptor antagonism
- 4 Intrinsic sympathomimetic activity
- 5 α1-Receptor antagonism
- 6 Other effects
- 7 Examples
- 7.1 Nonselective agents
- 7.2 β1-selective agents
- 7.3 β2-selective agents
- 7.4 β3-selective agents
- 8 Comparative information
- 8.1 Pharmacological differences
- 8.2 Indication differences
- 9 See also
- 10 References
- 11 External links
Medical uses
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:
- Angina pectoris[10][11]
- Atrial fibrillation[12]
- Cardiac arrhythmia
- Congestive heart failure
- Essential tremor
- Glaucoma
- Hypertension
- Migraine prophylaxis
- Mitral valve prolapse
- Myocardial infarction
- Phaeochromocytoma, in conjunction with α-blocker
- Postural orthostatic tachycardia syndrome
- Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism
- Theophylline overdose
Beta blockers have also been used for:
- Acute aortic dissection
- Hypertrophic obstructive cardiomyopathy
- Marfan syndrome (treatment with propranolol slows progression of aortic dilation and its complications)
- Prevention of variceal bleeding in portal hypertension
- Possible mitigation of hyperhidrosis
- Social 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 efficacy at reducing morbidity and mortality.[13][14][15] 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 known primarily for their reductive effect on heart rate, although this is not the only mechanism of action of importance in congestive heart failure[citation needed]. Beta blockers, in addition to their sympatholytic B1 activity in the heart, influence the renin–angiotensin system at the kidneys. Beta blockers cause a decrease in renin secretion, which in turn reduces the heart oxygen demand by lowering extracellular volume and increasing the oxygen-carrying capacity of blood. Beta blockers' sympatholytic activities reduce heart rate, thereby increasing the ejection fraction of the heart despite an initial reduction in ejection fraction.
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 number of hospital visits and hospitalizations were also reduced in the trials.[16]
Anxiety and performance enhancement
Officially, beta blockers are not approved for anxiolytic use by the U.S. Food and Drug Administration.[17] However, many controlled trials in the past 25 years indicate beta blockers are effective in anxiety disorders, though the mechanism of action is not known.[18] The physiological symptoms of the fight-or-flight response (pounding heart, cold/clammy hands, increased respiration, sweating, etc.) are significantly reduced, thus enabling anxious individuals to concentrate on the task at hand.
Musicians, public speakers, actors, and professional dancers have been known to use beta blockers to avoid performance anxiety, stage fright and tremor during both auditions and public performances. The application to stage fright was first recognized in The Lancet in 1976, and by 1987, a survey conducted by the International 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.[19] Beta blockers are inexpensive, said to be relatively safe and, on one hand, seem to improve musicians' performances on a technical level, while some, like 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."[19]
Since they promote lower heart rates and reduce tremors, beta blockers have been used in professional sports where high accuracy is required, including archery, shooting, golf[20] and snooker.[20] Beta blockers are banned by the International Olympic Committee.[21] A recent, high-profile transgression took place in the 2008 Summer Olympics, where 50 metre pistol silver medallist and 10 metre air pistol bronze medallist Kim Jong-su tested positive for propranolol and was stripped of his medals.
For similar reasons, beta blockers have also been used by stutterers[citation needed] and surgeons.[22]
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, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, 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.[23] Due to the high penetration across the blood–brain barrier, lipophilic beta blockers, such as propranolol and metoprolol, are more likely than other, less lipophilic, beta blockers to cause sleep disturbances, such as insomnia and vivid dreams and nightmares.[24]
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.
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally stimulate hepatic glycogen breakdown (glycogenolysis) and pancreatic release of glucagon, 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 tachycardia that serves as a warning sign for insulin-induced hypoglycemia may be masked. Therefore, beta blockers are to be used cautiously in diabetics.[25]
A 2007 study revealed 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.[26] 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.[27]
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.[28] The appropriate antihypertensive drugs to administer during hypertensive crisis resulting from stimulant abuse are vasodilators such as nitroglycerin, diuretics such as furosemide and alpha blockers such as phentolamine.[29]
Contraindications
Beta blockers are contraindicated in patients with asthma as stated in the British National Formulary 2011.[citation needed] They should also be avoided in patients with a history of cocaine use or in cocaine-induced tachycardia.[citation needed]
Beta blockers should not be used as a first-line treatment in the acute setting for cocaine-induced acute coronary syndrome (CIACS). No recent studies have been identified that show the benefit of beta blockers in reducing coronary vasospasm, or coronary vascular resistance, in patients with CIACS. In the multiple case studies identified, the use of beta blockers in CIACS resulted in detrimental outcomes, and the discontinuation of beta blockers used in the acute setting led to improvement in clinical course.[citation needed] The guidelines by the American College of Cardiology/American Heart Association also support this idea, and recommend against the use of beta blockers in cocaine-induced ST [expand acronym] elevation myocardial infarction (MI) because of the risk of coronary vasospasm.[citation needed] Though, in general, beta blockers improve mortality in patients who have suffered MI, it is unclear whether patients with CIACS will benefit from this mortality reduction because there are no studies assessing use of beta blockers in the long term, and because cocaine users may be prone to continue to abuse the substance, thus complicating the effect of drug therapy. [30]
Toxicity
Glucagon, used in the treatment of overdose,[31][32] increases the strength of heart contractions, increases intracellular cAMP, and decreases renal vascular resistance. It is therefore useful in patients with beta-blocker cardiotoxicity.[33][34] Cardiac pacing is usually reserved for patients unresponsive to pharmacological therapy.
Patients experiencing bronchospasm due to the β2 receptor-blocking effects of non-selective beta blockers may be treated with anticholinergic drugs, such as ipratropium, which are safer than beta agonists in patients with cardiovascular disease. Other antidotes for beta-blocker poisoning are salbutamol and isoprenaline.
β-Receptor antagonism
Stimulation of β1 receptors by epinephrine and norepinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity.[35] Stimulation of β1 receptors on the kidney causes renin release.[36] Stimulation of β2 receptors induces smooth muscle relaxation,[37] induces tremor in skeletal muscle,[38] and increases glycogenolysis in the liver and skeletal muscle.[39] Stimulation of β3 receptors induces lipolysis.[40]
Beta blockers inhibit these normal epinephrine and norepinephrine-mediated sympathetic actions,[6] but have minimal effect on resting subjects.[citation needed] That is, they reduce excitement/physical exertion on heart rate and force of contraction,[41] and also tremor[42] and breakdown of glycogen, but increase dilation of blood vessels[43] and constriction of bronchi.[44]
Therefore, nonselective beta blockers are expected to have antihypertensive effects.[45] The primary antihypertensive mechanism of beta blockers is unclear, but may involve reduction in cardiac output (due to negative chronotropic and inotropic effects).[46] It may also be due to reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity (for those beta 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. Negative chronotropic properties of beta blockers allow the lifesaving property of heart rate control. Beta blockers are readily titrated to optimal rate control in many pathologic states.
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
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). See partial agonist for a more general description.
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 after myocardial infarctions, 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.[23]
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 disturbances caused by some agents.[47]
They can also be used to treat glaucoma because they decrease intraocular pressure by lowering aqueous humor secretion.[48]
Examples
Dichloroisoprenaline, the first beta blocker.
Nonselective agents
- Alprenolol
- Bucindolol
- Carteolol
- Carvedilol (has additional α-blocking activity)
- Labetalol (has additional α-blocking activity)
- Nadolol
- Oxprenolol (has intrinsic sympathomimetic activity)
- Penbutolol (has intrinsic sympathomimetic activity)
- Pindolol (has intrinsic sympathomimetic activity)
- Propranolol
- Sotalol
- Timolol
- Eucommia bark (herb) [49]
β1-selective agents
Also known as cardioselective
- Acebutolol (has intrinsic sympathomimetic activity)
- Atenolol
- Betaxolol
- Bisoprolol
- Celiprolol
- Esmolol[50]
- Metoprolol
- Nebivolol (also increases nitric oxide release for vasodilation)
β2-selective agents
- Butaxamine (weak α-adrenergic agonist activity): No common clinical applications, but used in experiments.
- ICI-118,551: Highly selective β2-adrenergic receptor antagonist—no known clinical applications, but used in experiments due to its strong receptor specificity.
β3-selective agents
- SR 59230A (has additional α-blocking activity): Used in experiments.
Comparative information
Pharmacological differences
- Agents with intrinsic sympathomimetic action (ISA)
- Acebutolol, carteolol, celiprolol, mepindolol, oxprenolol, pindolol
- Agents with greater aqueous solubility (hydrophilic beta blockers)
- Atenolol, celiprolol, nadolol, sotalol
- Agents with membrane stabilizing effect
- Acebutolol, propranolol
Indication differences
- Agents specifically indicated for cardiac arrhythmia
- Esmolol, sotalol, landiolol
- Agents specifically indicated for congestive heart failure
- carvedilol, sustained-release metoprolol, bisoprolol, 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.[23]
See also
- Alpha blockers
References
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- ^ Stoschitzky K, Sakotnik A, Lercher P et al. (1999). "Influence of beta-blockers on melatonin release". Eur. J. Clin. Pharmacol. 55 (2): 111–115. doi:10.1007/s002280050604. PMID 10335905.
- ^ Shen, Howard (2008). Illustrated Pharmacology Memory Cards: PharMnemonics. Minireview. p. 15. ISBN 1-59541-101-1.
- ^ Greenway, F; Liu, Z; Yu, Y; Gupta, A (2011). "A clinical trial testing the safety and efficacy of a standardized Eucommia ulmoides Oliver bark extract to treat hypertension". Alternative medicine review 16 (4): 338–47. PMID 22214253.
- ^ Umehara S, Goyagi T, Nishikawa T, Tobe Y, Masaki Y (2010). "Esmolol and landiolol, selective beta1-adrenoreceptor antagonists, provide neuroprotection against spinal cord ischemia and reperfusion in rats". Anesthesia and Analgesia 21 (3): 1133–7. doi:10.1213/ANE.0b013e3181cdb06b. PMID 20103544.
External links
- Musicians and beta-blockers by Gerald Klickstein, March 11, 2010 (A blog post that considers "whether beta-blockers are safe, effective, and appropriate for performers to use.")
- 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)
- beta-Adrenergic Blockers at the US National Library of Medicine Medical Subject Headings (MeSH)
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UpToDate Contents
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- 1. β遮断剤の主な副作用 major side effects of beta blockers
- 2. 収縮能障害による心不全におけるβブロッカーの使用 use of beta blockers in heart failure due to systolic dysfunction
- 3. 安定狭心症のマネージメントにおけるβ遮断剤 beta blockers in the management of stable angina pectoris
- 4. 急性冠症候群：β遮断剤の役割 acute myocardial infarction role of beta blocker therapy
- 5. 収縮能障害による心不全におけるβブロッカー使用の理論的根拠および臨床試験 rationale for and clinical trials of beta blockers in heart failure due to systolic dysfunction
English Journal
- Angiotensin II AT1 receptor blockers as treatments for inflammatory brain disorders.
- Saavedra JM.SourceSection on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, U.S.A.
- Clinical science (London, England : 1979).Clin Sci (Lond).2012 Nov 1;123(10):567-90.
- The effects of brain AngII (angiotensin II) depend on AT1 receptor (AngII type 1 receptor) stimulation and include regulation of cerebrovascular flow, autonomic and hormonal systems, stress, innate immune response and behaviour. Excessive brain AT1 receptor activity associates with hypertension and
- PMID 22827472
- Effects of the aquatic contaminant human pharmaceuticals and their mixtures on the proliferation and migratory responses of the bioindicator freshwater ciliate Tetrahymena.
- Láng J, Kőhidai L.SourceDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, PO Box 370, H-1445 Budapest, Hungary.
- Chemosphere.Chemosphere.2012 Oct;89(5):592-601. Epub 2012 Jun 12.
- An increasing attention is paid to the potential harmful effects of aquatic contaminant pharmaceuticals exerted on both biosystems and humans. In the present work the effects of 14 pharmaceuticals including NSAIDs, antibiotics, β-blockers and a frequently used X-ray contrast media on the proliferat
- PMID 22698373
Japanese Journal
- Improved Long-Term Prognosis of Dilated Cardiomyopathy With Implementation of Evidenced-Based Medication – Report From the CHART Studies –
- , , , , , , , , , , , , ,on behalf of the CHART-2 Investigators
- Circulation Journal 79(6), 1332-1341, 2015
- … The use of β-blockers and aldosterone antagonists was significantly increased, while that of loop diuretics and digitalis was significantly decreased in the CHART-2 Study. …
- NAID 130005073161
- 交感神経の活動亢進が疑われた維持血液透析患者の繰り返す急性心不全の1例
- 西川 真那,宮川 一也,玉田 直己,前川 浩一,三木 隆
- 日本透析医学会雑誌 48(5), 303-308, 2015
- 50歳女性, 血液透析 (HD) 歴6年. 急性心不全で入院しdry weightの減量と降圧薬の調整を行い退院した. 退院4日後に突然の呼吸苦が出現し, 血圧263/99mmHg, 脈拍109bpm, SpO2 (室内気) 41%であった. 胸部単純写真は肺水腫像であったが, 心エコーでは明らかな体液過剰はなく拡張障害を認めた. 動静脈の収縮による体液の末梢から心肺へのシフト (vascular …
- NAID 130005072760
- Beta-blocker Treatment Does Not Worsen Critical Limb Ischemia in Patients Receiving Endovascular Therapy
- , , , , ,
- Journal of Atherosclerosis and Thrombosis 22(5), 481-489, 2015
- … Aim: It has been reported that beta-blockers (BB) reduce cardiovascular events in patients with atherosclerotic disease. … We investigated whether beta-blocker therapy affects the clinical outcomes of CLI patients.Methods: Between March 2004 and December 2011, 1,873 consecutive CLI patients who received endovascular therapy (EVT) (394 BB-treated patients and 1,479 non-BB-treated patients) for de novo infrainguinal lesions were identified retrospectively. …
- NAID 130005071049
Related Links
- Learn about the side effects and uses of beta blockers, a drug that treats angina, heart failure, migraines, high blood pressure, anxiety, and tremors. Generic and brand names are included in the article.
- Beta Blockers Definition Beta blockers are medicines that affect the body's response to certain nerve impulses. This, in turn, decreases the force and rate of the heart's contractions, which lowers blood pressure and reduces the heart ...
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