64-411: Atenolol is a beta blocker medication primarily used to treat high blood pressure and heart-associated chest pain . Although used to treat high blood pressure, it does not seem to improve mortality in those with the condition. Other uses include the prevention of migraines and treatment of certain irregular heart beats . It is taken orally (by mouth) or by intravenous injection (injection into
128-411: A beta blocker like atenolol to MAOI therapy is safe and effective for improving orthostatic hypotension with MAOIs. Atenolol is a beta blocker ; that is, an antagonist of the β-adrenergic receptors . It is specifically a selective antagonist of the β 1 -adrenergic receptor with no intrinsic sympathomimetic activity (i.e., partial agonist activity) or membrane-stabilizing activity . However,
192-406: A class of medications that are predominantly used to manage abnormal heart rhythms ( arrhythmia ), and to protect the heart from a second heart attack after a first heart attack ( secondary prevention ). They are also widely used to treat high blood pressure , although they are no longer the first choice for initial treatment of most people. Beta blockers are competitive antagonists that block
256-431: A constricting effect on the bronchi of the lungs, possibly worsening or causing asthma symptoms. Since β 2 adrenergic receptors can cause vascular smooth muscle dilation, beta blockers may cause some vasoconstriction. However, this effect tends to be small because the activity of β 2 receptors is overshadowed by the more dominant vasoconstricting α 1 receptors. By far the greatest effect of beta blockers remains in
320-454: A decrease in renin secretion, which in turn reduces the heart oxygen demand by lowering the extracellular volume 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
384-604: A diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Plasma levels are usually less than 3 mg/L during therapeutic administration, but can range from 3–30 mg/L in overdose victims. Interactions with atenolol include catecholamine-depleting drugs like reserpine , calcium channel blockers , disopyramide , amiodarone , clonidine , prostaglandin synthase inhibitors like indomethacin , and digitalis glycosides . Most of these interactions involve either additive cardiovascular effects or reduction of atenolol's effects. Atenolol
448-412: A further decrease in ejection fraction, worsening the patient's current symptoms. 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. Beta blockers, in addition to their sympatholytic β 1 activity in the heart, influence the renin–angiotensin system at the kidneys. Beta blockers cause
512-525: 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. Beta blockers are indicated for the treatment of acute myocardial infarctions . During a myocardial infarction, systemic stress causes an increase in circulating catecholamines . This results an increase in heart rate and blood pressure, therefore increasing myocardial oxygen demand. Beta blockers competitively inhibit catecholamines acting on
576-505: A patient with diabetes mellitus on beta blockers. Abrupt withdrawal can result in a thyroid storm . 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
640-480: A relevant clinical choice for treating some conditions, since beta blockers are a diverse group of medicines with different properties that still requires further research. As consequence, reasons for the popularity of beta blockers cannot be fully attributed to a slow healthcare system – patient compliance factor, such as treatment cost and duration, also affect adherence and popularity of therapy. Beta blocker Beta blockers , also spelled β-blockers , are
704-420: A single oral dose. The general effects of atenolol, including beta-blocking and antihypertensive effects, last for at least 24 hours following oral doses of 50 or 100 mg. With intravenous administration, maximal reduction in exercise-related tachycardia occurs within 5 minutes and following a single 10 mg dose has dissipated within 12 hours. The duration of action of atenolol
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#1732780007923768-475: 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". Low certainty evidence indicates that the use of beta blockers around the time of cardiac surgery may decrease the risk of heart dysrhythmias and atrial fibrillation . Starting them around
832-497: A vein). It can also be used with other blood pressure medications . Common side effects include feeling tired , heart failure , dizziness , depression , and shortness of breath . Other serious side effects include bronchial spasm . Use is not recommended during pregnancy and alternative drugs are preferred when breastfeeding . It works by blocking β 1 -adrenergic receptors in the heart , thus decreasing heart rate , force of heart beats , and blood pressure . Atenolol
896-399: Is 6 to 16%. Atenolol is classified as a beta blocker with low lipophilicity and hence lower potential for crossing the blood–brain barrier and entering the brain. This in turn may result in fewer effects in the central nervous system as well as a lower risk of neuropsychiatric side effects. Only small amounts of atenolol are said to enter the brain. The brain-to-blood ratio of atenolol
960-564: Is also available in the form of oral tablets containing a combination of 50 or 100 mg atenolol and 50 mg chlortalidone . Atenolol was previously available in a 0.5 mg/mL solution for injection as well, but this formulation was discontinued. Hypertension treated with a β-blocker such as atenolol, alone or in conjunction with a thiazide diuretic, is associated with a higher incidence of new onset type 2 diabetes mellitus compared to those treated with an ACE inhibitor or angiotensin receptor blocker. β-blockers, of which atenolol
1024-713: Is also commonly associated with orthostatic hypotension . Carvedilol therapy is commonly associated with edema . 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, vivid dreams and nightmares. Adverse effects associated with β 2 -adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with β 1 -selective (often termed "cardioselective") agents, but receptor selectivity diminishes at higher doses. Beta blockade, especially of
1088-468: Is also structurally related to the catecholamine neurotransmitters epinephrine (adrenaline) and norepinephrine (noradrenaline). Atenolol has been given as an example of how slow healthcare providers are to change their prescribing practices in the face of medical evidence that indicates that a drug is not as effective as others in treating some conditions. In 2012, 33.8 million prescriptions were written to American patients for this drug. In 2014, it
1152-724: Is dose-related and is correlated with circulating levels of atenolol. The oral bioavailability of atenolol is approximately 50 to 60%. The absorption of atenolol with oral administration is rapid and consistent but is incomplete. About 50% of an oral dose of atenolol is absorbed from the intestines , with the rest excreted in feces . Maximal concentrations of atenolol occur 2 to 4 hours following an oral dose, whereas peak concentrations occur within 5 minutes with intravenous administration . The pharmacokinetic profile of atenolol results in it having relatively consistent plasma drug levels with about 4-fold variation between individuals. The plasma protein binding of atenolol
1216-526: Is excreted about 40 to 50% in urine and 50% in feces with oral administration. Conversely, it is excreted 85 to 100% in urine unchanged and 10% in feces with intravenous administration. Only very small amounts of hydroxyatenolol and atenolol glucuronide are found in urine with atenolol. The elimination half-life of atenolol is about 6 to 7 hours. The half-life of atenolol does not change with continuous administration. With intravenous administration, atenolol levels rapidly decline (5- to 10-fold) during
1280-426: Is largely symptomatic. Hospitalization and intensive monitoring is indicated. Activated charcoal is useful to absorb the drug. Atropine will counteract bradycardia, glucagon helps with hypoglycemia, dobutamine can be given against hypotension and the inhalation of a β 2 -mimetic such as hexoprenalin or salbutamol will terminate bronchospasms. Blood or plasma atenolol concentrations may be measured to confirm
1344-525: Is mainly eliminated renally without being metabolized by the liver or by cytochrome P450 enzymes . As a result, it has little or no potential for cytochrome P450-related drug interactions, for instance with inhibitors and inducers of these enzymes. Accordingly, the broad/ non-selective cytochrome P450 inhibitor cimetidine had no effect on atenolol levels, whereas cimetidine has been found to significantly increase metoprolol and propranolol levels. Beta blockers like atenolol can reduce or block
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#17327800079231408-613: Is mainly studied, provides weaker protection against stroke and mortality in patients over 60 years old compared to other antihypertensive medications. Diuretics may be associated with better cardiovascular and cerebrovascular outcomes than β-blockers in the elderly. Rarely, atenolol has been associated with induction of acute delirium . Symptoms of overdose are due to excessive pharmacodynamic actions on β 1 and also β 2 -receptors. These include bradycardia (slow heartbeat), severe hypotension with shock , acute heart failure , hypoglycemia and bronchospastic reactions. Treatment
1472-542: 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 , labetalol and acebutolol ) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low-level agonist activity at
1536-478: Is usually reserved for patients unresponsive to pharmacological therapy . People experiencing bronchospasm due to the β 2 receptor-blocking effects of nonselective 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 . Also referred to as intrinsic sympathomimetic effect, this term
1600-402: The cardiovascular effects of sympathomimetics and amphetamines , such as hypertension and tachycardia . Atenolol has been found to be safe in combination with the non-selective monoamine oxidase inhibitor (MAOI) phenelzine and actually improved orthostatic hypotension and hypertensive reactions with phenelzine. However, more research is still needed to assess whether addition of
1664-413: The liver and skeletal muscle . Stimulation of β 3 receptors induces lipolysis . Beta blockers inhibit these normal epinephrine- and norepinephrine-mediated sympathetic actions, but have minimal effect on resting subjects. That is, they reduce the effect of excitement or physical exertion on heart rate and force of contraction, and also tremor, and breakdown of glycogen. Beta blockers can have
1728-413: The nonselective β-blocker-induced worsening asthma and/or COPD. Epinephrine signals early warning of the upcoming hypoglycemia . Beta blockers' inhibition on epinephrine's effect can somewhat exacerbate hypoglycemia by interfering with glycogenolysis and mask signs of hypoglycemia such as tachycardia, palpitations, diaphoresis , and tremors. Diligent blood glucose level monitoring is necessary for
1792-437: The 20th century. For the treatment of primary hypertension, meta-analyses of studies which mostly used atenolol have shown that although beta blockers are more effective than placebo in preventing stroke and total cardiovascular events, they are not as effective as diuretics , medications inhibiting the renin–angiotensin system (e.g., ACE inhibitors ), or calcium channel blockers . Beta blockers are utilized in
1856-471: The alpha-adrenergic system stimulation unopposed. Beta blockers with lipophilic properties and CNS penetration such as metoprolol and labetalol may be useful for treating CNS and cardiovascular toxicity from a methamphetamine overdose. The mixed alpha- and beta blocker labetalol is especially useful for treatment of concomitant tachycardia and hypertension induced by methamphetamine. The phenomenon of "unopposed alpha stimulation" has not been reported with
1920-550: 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 β 2 -adrenoceptors normally stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release of the hormone glucagon , which work together to increase plasma glucose. Therefore, blocking β 2 -adrenoceptors lowers plasma glucose. β 1 -blockers have fewer metabolic side effects in diabetic patients; however,
1984-407: The binding to the receptor of epinephrine and other stress hormones and weaken the effects of stress hormones. In 1964, James Black synthesized the first clinically significant beta blockers— propranolol and pronethalol ; it revolutionized the medical management of angina pectoris and is considered by many to be one of the most important contributions to clinical medicine and pharmacology of
Atenolol - Misplaced Pages Continue
2048-410: The case of propranolol. Two metabolites of atenolol have been identified: hydroxyatenolol and atenolol glucuronide. It has been said that it is unknown if these metabolites are active. However, another source stated that hydroxyatenolol has one-tenth the beta-blocking activity of atenolol. Instead of by hepatic metabolism, atenolol is eliminated from the blood mainly via renal excretion . Atenolol
2112-553: 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. Glucagon , used in the treatment of overdose, increases the strength of heart contractions, increases intracellular cAMP , and decreases renal vascular resistance . It is, therefore, useful in patients with beta blocker cardiotoxicity. Cardiac pacing
2176-405: The efficiency of cardiac contraction and contribute to the low ejection fraction. Beta blockers counter this inappropriately high sympathetic activity, eventually leading to an improved ejection fraction, 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,
2240-569: The fast heart rate that serves as a warning sign for insulin-induced low blood sugar may be masked, resulting in hypoglycemia unawareness . This is termed beta blocker-induced hypoglycemia unawareness . Therefore, beta blockers are to be used cautiously in diabetics. A 2007 study revealed diuretics and beta blockers used for hypertension increase a patient's risk of developing diabetes mellitus , while ACE inhibitors and angiotensin II receptor antagonists (angiotensin receptor blockers) actually decrease
2304-416: The first 7 hours and thereafter decline at a rate similar to that with oral administration. The elimination of atenolol is slowed in renal impairment , with the elimination rate being closely related to the glomerular filtration rate (GFR) and with significant accumulation occurring when the creatinine clearance rate is under 35 mL/min/1.73 m. At a GFR of less than 10 mL/min,
2368-424: The half-life of atenolol increases up to 36 hours. Atenolol is a substituted phenethylamine derivative . It is specifically β-phenylethylamine with an α-keto substitution and a 4- substitution on the phenyl ring . The experimental log P of atenolol is 0.16 and its predicted log P ranges from −0.03 to 0.57. Atenolol is closely structurally related to metoprolol and certain other beta blockers. It
2432-541: The heart and in the kidneys. β 2 -adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. β 3 -adrenergic receptors are located in fat cells. 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
2496-431: The heart. Newer, third-generation beta blockers can cause vasodilation through blockade of alpha-adrenergic receptors. Accordingly, nonselective beta blockers are expected to have antihypertensive effects. The primary antihypertensive mechanism of beta blockers is unclear, but may involve reduction in cardiac output (due to negative chronotropic and inotropic effects). It may also be due to reduction in renin release from
2560-566: 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. Activated charcoal Too Many Requests If you report this error to
2624-461: The management of angina and tachyarrhythmia . Stimulation of β 1 receptors by epinephrine and norepinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β 1 receptors on the kidney causes renin release. Stimulation of β 2 receptors induces smooth muscle relaxation, induces tremor in skeletal muscle , and increases glycogenolysis in
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2688-514: The mechanism of action is not known. 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
2752-430: The numbers of hospital visits and hospitalizations were also reduced in the trials. 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. Therapeutic administration of beta blockers for congestive heart failure ought to begin at very low doses ( 1 ⁄ 8 of target) with
2816-607: The possibility of "unopposed α-stimulation" with selective beta blockers. Because 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 and snooker . Beta blockers are banned in some sports by the International Olympic Committee . In the 2008 Summer Olympics , 50-metre pistol silver medalist and 10-metre air pistol bronze medalist Kim Jong-su tested positive for propranolol and
2880-662: The preferential action of atenolol is not absolute, and at high doses. it can also block β 2 -adrenergic receptors . Beta-blocking effects of atenolol include reduction in resting and exercise heart rate and cardiac output , reduction of systolic and diastolic blood pressure at rest and with exercise, inhibition of tachycardia induced by isoproterenol (a non-selective β-adrenergic receptor agonist ), and reduction of reflex orthostatic tachycardia. The beta-blocking effects of atenolol, as measured by reduction of exercise-related tachycardia, are apparent within 1 hour and are maximal within 2 to 4 hours following
2944-481: The receptor sites for the endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) on adrenergic beta receptors , of the sympathetic nervous system , which mediates the fight-or-flight response . Some block activation of all types of β-adrenergic receptors and others are selective for one of the three known types of beta receptors, designated β 1 , β 2 and β 3 receptors. β 1 -adrenergic receptors are located mainly in
3008-416: The risk of bradycardia. A 2014 Cochrane review investigated the use of beta blockers in the maintenance of chronic type B thoracic aortic aneurysm in comparison to other anti hypertensive medications. The review found no suitable evidence to support the current guidelines recommending its use. A 2017 Cochrane review on the use of beta blockers to prevent aortic dissections in people with Marfan syndrome
3072-614: The risk of diabetes. 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. Beta blockers must not be used in the treatment of selective alpha-adrenergic agonist overdose. The blockade of only beta receptors increases blood pressure , reduces coronary blood flow, left ventricular function , and cardiac output and tissue perfusion by means of leaving
3136-562: The symptoms of alcohol withdrawal . The role for β-blockers in general in hypertension was downgraded in June 2006 in the United Kingdom, and later in the United States, as they are less appropriate than other agents such as ACE inhibitors , calcium channel blockers , thiazide diuretics and angiotensin receptor blockers , particularly in the elderly. Atenolol is available in the form of 25, 50, and 100 mg oral tablets . It
3200-457: 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. Low-certainty evidence suggests that beta blockers used perioperatively in non-cardiac surgeries may increase
3264-808: The treatment of anxiety states, cases of thyrotoxicosis, glaucoma, migraines, and esophageal varices. Although beta blockers were once contraindicated in congestive 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. Bisoprolol , carvedilol , and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy 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
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#17327800079233328-431: The treatment of hypertension. 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. 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. A 2017 Cochrane review on
3392-565: 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,
3456-507: The use of beta blockers for treatment of methamphetamine toxicity. Other appropriate antihypertensive drugs to administer during hypertensive crisis resulting from stimulant overdose are vasodilators such as nitroglycerin , diuretics such as furosemide , and alpha blockers such as phentolamine . Relative contraindications, or contraindications specific to certain beta-blockers: Cautions: The 2007 National Heart, Lung, and Blood Institute ( NHLBI ) asthma guidelines recommend against
3520-462: The use of beta blockers in hypertension found a modest reduction in cardiovascular disease but little to no change in mortality It suggested that the effects of beta blockers are inferior to other anti-hypertensive medications. Officially, beta blockers are not approved for anxiolytic use by the U.S. Food and Drug Administration . However, many controlled trials in the past 25 years indicate beta blockers are effective in anxiety disorders , though
3584-430: The use of non-selective beta blockers in asthmatics, while allowing for the use of cardio selective beta blockers. Cardio selective beta blocker (β 1 blockers) can be prescribed at the least possible dose to those with mild to moderate respiratory symptoms. β2-agonists can somewhat mitigate β-blocker-induced bronchospasm where it exerts greater efficacy on reversing selective β-blocker-induced bronchospasm than
3648-556: The β 1 -adrenergic receptors, thus reducing these detrimental effects and resulting in reduced myocardial oxygen consumption and demand. A 2019 Cochrane review compared beta blockers with placebo or no intervention, it found that beta blockers probably reduced the short-term risk of reinfarction and the long-term risk of all-cause mortality and cardiovascular mortality. The review identified that beta blockers likely had little to no impact on short-term all-cause mortality and cardiovascular mortality. Beta blockers are widely used for
3712-400: 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 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
3776-476: Was 0.2 : 1 in one study, whereas the ratio for propranolol was 33 : 1 in the same study. Atenolol undergoes minimal or negligible metabolism by the liver . It has been estimated that about 5% of atenolol is metabolized. This is in contrast to other beta blockers like propranolol and metoprolol , but is similar to nadolol . In accordance with its lack of hepatic metabolism, the pharmacokinetics of atenolol are not altered in hepatic impairment , unlike
3840-565: 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. Beta blockers are inexpensive, said to be relatively safe, and on one hand, seem to improve musicians' performances on
3904-438: Was in the top (most common) 1% of drugs prescribed to Medicare patients. Although the number of prescriptions has been declining steadily since limited evidence articles contesting its efficacy was published, it has been estimated that it would take 20 years for doctors to stop prescribing it for hypertension. Despite its diminished efficacy when compared to newer antihypertensive drugs , atenolol and other beta blockers are still
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#17327800079233968-597: Was patented in 1969 and approved for medical use in 1975. It is on the World Health Organization's List of Essential Medicines . It is available as a generic medication . In 2022, it was the 63rd most commonly prescribed medication in the United States, with more than 10 million prescriptions. Atenolol is used for a number of conditions including hyperthyroidism , hypertension , angina , long QT syndrome , acute myocardial infarction , supraventricular tachycardia , ventricular tachycardia , and
4032-680: Was stripped of his medals. For similar reasons, beta blockers have also been used by surgeons. Classical musicians have commonly used beta blockers since the 1970s to reduce stage fright . Adverse drug reactions 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 , alteration of glucose and lipid metabolism . Mixed α 1 /β-antagonist therapy
4096-939: Was unable to draw definitive conclusions due to lack of evidence. Adrenergic antagonists are mostly used for cardiovascular disease . The adrenergic antagonists are widely used for lowering blood pressure and relieving hypertension . These antagonists have a been proven to relieve the pain caused by myocardial infarction , and also the infarction size, which correlates with heart rate. There are few non-cardiovascular uses for adrenergic antagonists. Alpha-adrenergic antagonists are also used for treatment of ureteric stones , pain and panic disorders , withdrawal , and anesthesia . Beta blockers are used to treat acute cardiovascular toxicity (e.g. in overdose ) caused by sympathomimetics , for instance caused by amphetamine , methamphetamine , cocaine , ephedrine , and other drugs. Combined α 1 and beta blockers like labetalol and carvedilol may be more favorable for such purposes due to
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