アテノロール

0.16

log Kow= 0.16

0.16

White, crystalline powder

Crystals from ethyl acetate

Colorless crystals

13300

Freely soluble in methanol; soluble in acetic acid, DMSO; sparingly soluble in 96% ethanol; slightly soluble in isopropanol; very slightly soluble in acetone, dioxane; practically insoluble in acetonitrile, ethyl acetate; chloroform

Freely soluble in 1 N HCl (300 mg/ml @ 25 °C); less soluble in chloroform (3 mg/ml @ 25 °C)

In water, 1.33X10+4 mg/l @ 25 °C

13.3 mg/mL at 25 °C

>40 [ug/mL] (The mean of the results at pH 7.4)

158-160

146 - 148 °C

147 °C

Positive

4.95

2.7

Agilent XCT

Electrospray ionization

formic acid (5.3nM)

9.58

9.54

9.6

9.6

pKa = 9.6

157.8 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID2022628]；157.9 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: APCI+; Dataset: TOXCAST; Source Identifier: DTXSID2022628]；164.2 Ų [M+Na]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID2022628]

155.32 Ų [M+H-H2O]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]；158.38 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]；165.83 Ų [M+K]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]；163.26 Ų [M+Na]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

159.5 Ų [M+H]+ [CCS Type: TW; Method: Major Mix IMS/Tof Calibration Kit (Waters)]

159 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

This chemical does not meet GHS hazard criteria for 3.4% (3 of 89) of reports.

Warning

H302 (79.8%): Harmful if swallowed [Warning Acute toxicity, oral]；H319 (67.4%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]；H351 (64%): Suspected of causing cancer [Warning Carcinogenicity]；H362 (74.2%): May cause harm to breast-fed children [Reproductive toxicity, effects on or via lactation]

P203, P260, P263, P264, P264+P265, P270, P280, P301+P317, P305+P351+P338, P318, P330, P337+P317, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 89 reports by companies from 24 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.；Reported as not meeting GHS hazard criteria per 3 of 89 reports by companies.；There are 22 notifications provided by 86 of 89 reports by companies with hazard statement code(s).；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

Hazard Traits - Developmental Toxicity；Authoritative List - Prop 65；Report - regardless of intended function of ingredient in the product

Atenolol: Does not have an individual approval but may be used under an appropriate group standard

Atenolol, used as a beta adrenergic blocking agent, was approved by FDA for marketing in the United States 8/81.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed drug products, incl atenolol, approved on the basis of safety and effectiveness by FDA under sections 505 and 507 of the Federal Food, Drug, and Cosmetic Act.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

Acute Tox. 4 (79.8%)；Eye Irrit. 2 (67.4%)；Carc. 2 (64%)；Lact. (74.2%)

Repr. 1A (100%)；Lact. (100%)；Aquatic Chronic 2 (100%)

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Concomitant administration of atenolol with reserpine may increase the incidence of hypotension and bradycardia as compared with atenolol alone, because of reserpine's catecholamine-depleting activity. Atenolol also is additive with and may potentiate the hypotensive actions of other hypotensive agents (e.g., hydralazine, methylodpa).

It has been shown that paradoxical pressor response to a beta adrenoceptor antagonist occurs in conscious rats pretreated with an alpha adrenoceptor antagonist. This study examines the influence of anaesthetic agents on mean arterial pressure response to a beta blocker. ... IV injections of all three beta blockers caused dose dependent increases in mean arterial pressure in urethane anesthetized rats. In halothane anesthetized rats, propranolol and atenolol did not alter mean arterial pressure ... In the presence of pentobarbitone, none of the beta blockers raised mean arterial pressure. ... /When/ propranolol or atenolol were iv injected in pentobarbitone anesthetized rats treated with both phentolamine and adrenaline, /they both/ ... raised the mean arterial pressure. /These/ results show that anesthetic agents differentially affect the mean arterial pressure response to a beta blocker.

In a recent study in which metabolic characteristics of newly detected obese and nonobese hypertensive subjects were compared with those of normotensive subjects, insulin sensitivity was decreased, fasting insulin values and insulin values after an intravenous glucose tolerance test were increased, and fasting and intravenous glucose tolerance glucose values were increased in both hypertensive groups. ... The effects of various antihypertensive agents on these metabolic variables have been assessed in prospective trials. Treatment with the beta 1 selective blocking agents metoprolol and atenolol was associated with decreased insulin sensitivity and increased fasting values of insulin and glucose.

A double blind, randomized, crossover study of the pharmacokinetics of nifedipine and atenolol was conducted in 15 healthy male subjects (mean age 32 yr) who received a single oral tablet containing 50 mg atenolol, a sustained action tablet containing 20 mg nifedipine, both the atenolol and nifedipine tablets together, or an oral capsule containing 50 mg atenolol and 20 mg sustained release nifedipine. There was no difference between atenolol alone, given with nifedipine tablet or in the combination tablet with respect to time to maximum blood concentration or elimination half-life. ... /In conclusion,/ the fixed combination of nifedipine and atenolol is bioequivalent to the free combination and the bioavailability of both drugs in the fixed combination is equivalent to that of the single tablets.

For more Interactions (Complete) data for ATENOLOL (14 total), please visit the HSDB record page.

Atenolol therapy has been associated with mild-to-moderate elevations of serum aminotransferase levels in 1% to 2% of patients. These elevations, however, are usually asymptomatic and transient and resolve even with continuation of therapy. A few instances of clinically apparent, acute liver injury attributable to atenolol have been reported. In view of its wide scale use, atenolol induced liver injury is exceedingly rare. The onset of injury has been within 1 to 4 weeks and pattern of liver enzyme elevations has been hepatocellular or mixed. Symptoms of hypersensitivity (rash, fever, eosinophilia) are uncommon as is autoantibody formation. Most cases are self-limiting and resolve rapidly once atenolol is stopped; however, at least one fatal instance has been reported.；Likelihood score: D (Possible rare cause of clinically apparent liver injury).

According to product labeling, the adverse effects of atenolol are listed below.；* Common adverse effects include bradycardia, diarrhea, dizziness, constipation, confusion, dyspnea, headache, heart failure, erectile dysfunction, nausea, fatigue, paraesthesia, peripheral coldness, rash, sleep disorders, syncope, visual impairment, and bronchospasm.；* Rare adverse effects include alopecia, dry mouth, postural hypotension, psychosis, psoriasis, thrombocytopenia, depression, mild transaminitis, and depression.；* The BRASH syndrome is characterized by severe bradycardia, renal failure, atrioventricular blockade, shock, and hyperkalemia. If suspicion of BRASH syndrome exists, discontinuation of atenolol is recommended.；Drug-Drug Interactions；* Caution is advised when using rivastigmine concurrently with β-blockers such as atenolol, especially in patients with sick sinus syndrome or cardiovascular comorbidities due to the risk of syncope and bradycardia.；* Administering atenolol concurrently with amiodarone, digoxin, or verapamil may cause heart block, bradycardia, and left ventricular dysfunction.；* Antipsychotics and β-blockers have the potential for interactions. A case report documenting bradycardia induced by the combination of risperidone and atenolol has been published.；* As amifostine can cause a rapid drop in blood pressure, it is advisable to avoid concurrently using blood pressure–lowering agents, including atenolol, with amifostine.；* As the American Academy of Family Physicians (AAFP) guidelines recommend, β-blockers, such as atenolol, should be tapered and discontinued several days before discontinuing clonidine to reduce the risk of rebound hypertension.

Atenolol is distributed into milk. The drug distributes into milk in concentrations 1.5-6.8 times those in maternal serum. In addition, adverse beta-adrenergic effects (eg, bradycardia) and potentially toxic serum atenolol concentrations (2 ug/ml 48 hours after discontinuance of breast feeding in at least one infant) can occur.

Signs and Symptoms of Overdose；Symptoms of atenolol toxicity may include bradycardia, lethargy, hypotension, respiratory drive disorders, hypothermia, hypoglycemia, and seizures.；Management of Overdose；The treatment for β-blocker toxicity is primarily supportive. If administered orally, any unabsorbed drug can be removed by gastric lavage or activated charcoal (within 1 to 2 hours). Hemodialysis is effective in eliminating atenolol from the general systemic circulation. Inotropes and chronotropes, such as IV epinephrine and atropine, are recommended for treating severe bradycardia. Usually, atropine is administered as a 0.5-mg IV or intraosseous bolus and may be repeated every 3 to 5 minutes, up to a total dose of 3 mg. A transvenous cardiac pacemaker may also be utilized in refractory cases or for treating second- or third-degree heart block.；A titrated glucagon bolus at a dose of 50 mcg/kg can improve myocardial contractility and atrioventricular conduction and increase heart rate in patients. Continuous blood pressure monitoring is imperative, and vasopressors such as norepinephrine (levarterenol) may be considered in hypotension. A β-2 agonist such as aminophylline or isoproterenol may alleviate symptoms for patients with bronchospasm. In cases refractory to the standard treatment, high-dose insulin euglycemic therapy, initiated with a 1 unit/kg bolus followed by a 1 unit/kg/h drip, may be considered to manage overdose under the guidance of a toxicologist.；Lignocaine can be used in the management of arrhythmias resulting from β-blocker toxicity. Veno-arterial extracorporeal membrane oxygenation is also associated with reduced mortality. For asymptomatic β-1-blocker overdoses, monitoring the patient for at least 6 hours is recommended.

Like metoprolol, atenolol competes with sympathomimetic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting sympathetic stimulation. This results in a reduction in resting heart rate, cardiac output, systolic and diastolic blood pressure, and reflex orthostatic hypotension. Higher doses of atenolol also competitively block beta(2)-adrenergic responses in the bronchial and vascular smooth muscles.

/HUMAN EXPOSURE STUDIES/ A case of severe bradycardia, hypotension and marked hyperglycemia in a 15 yr old girl who ingested 10 oral tablets of 50 mg atenolol in a suicide attempt is reported. The patient was treated with gastric lavage and activated charcoal 60 g; no tablets were recovered in the lavage fluid. After an iv infusion of 5% dextrose was started, the patient's blood glucose increased to 90 mg/dl. She was given atropine sulfate 0.5 mg iv for hemodynamic support. It was concluded that, because of the severe and prolonged toxicity in this patient after a minimal overdose, caution is warranted in dealing with atenolol overdose.

/HUMAN EXPOSURE STUDIES/ To compare the effects of uteroplacental circulation of two beta adrenoceptor blockers, atenolol (cardioselective) and pindolol (non-selective with intrinsic sympathomimetic activity). Design: Controlled double blind double dummy study, ...29 women with pregnancy induced hypertension in the third trimester /were/ randomized to atenolol /13/ and to pindolol /16/. ...Pulsatility index in fetal aorta, umbilical artery, and maternal arcuate artery, volumetric blood flow in fetal aorta and umbilical vein /were measured/. /The/ mean arterial blood pressure decreased by 9.0 (95% confidence interval -13.0 to -5.0) mm Hg in the atenolol group and by 7.8 (-11.4 to -4.2) mm Hg in the pindolol group. During atenolol treatment the pulsatility index increased significantly from 1.82 (standard deviation 0.20) to 2.07 (0.32) in the fetal thoracic descending aorta, from 1.44 (0.28) to 1.79 (0.27) in the abdominal aorta, and from 0.93 (0.17) to 1.05 (0.19) in the umbilical artery; the volumetric blood flow in the umbilical vein decreased from 106 (28.8) to 84 (22.6) ml/min/kg. No such changes were seen after treatment with pindolol. Birth weight was similar in the two groups but placental weight was significantly different 529 (122) g in atenolol group v 653 (136) g in pindolol group; p=0.03). /In conclusion,/ the hypotensive effect was similar with both drugs, but only the beta 1-blocker atenolol had significant effects on fetal hemodynamics, although within normal ranges. The implications of these findings can be only speculative, but negative fetal consequences of beta 1-adrenoceptor blockade cannot be excluded.

/HUMAN EXPOSURE STUDIES/ To compare the obstetric and fetal outcome between women receiving atenolol (as monotherapy) and other antihypertensive drug monotherapies, and also to investigate the effect of duration of treatment on fetal growth, we performed a retrospective cohort study of 312 pregnancies in 223 women ... Atenolol (as monotherapy) was given in 78 pregnancies (25.0%), other types of antihypertensive drugs as monotherapy were given in 53 pregnancies (17.0%), and multiple drug combinations were given in 90 pregnancies (28.8%). In 91 pregnancies (29.2%) no antihypertensive drugs were given. Atenolol was found to be associated with lower birth weight and ponderal index values, with a trend toward a higher prevalence of preterm (<37 weeks) delivery and small-for-gestational-age babies when compared to other antihypertensive drugs as monotherapy, or to no treatment.

Drug Induced Liver Injury Rank (DILIrank 2.0)

Atenolol

vLess-DILI-concern

4

Adverse reactions

DOI:10.1016/j.drudis.2016.02.015

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Chronic studies employing oral atenolol performed in animals have revealed the occurrence of vacuolation of epithelial cells of Brunner's glands in the duodenum of both male and female dogs at all tested dose levels of atenolol (starting at 15 mg/kg/day...) and increased incidence of atrial degeneration of hearts of male rats at 300 but not 150 mg atenolol/kg/day.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ No evidence of carcinogenicity was observed following administration of atenolol at dosages up to 300 mg/kg daily... for 18 months in mice or 18 or 24 months in rats. However, an increased of benign adrenal medullary tumors in males and females, mammary fibroadenomas in females, and anterior pituitary adenomas and thyroid parafollicular cell carcinomas in males was observed at 24 months in rats receiving 500-1,500 mg/kg of atenolol daily.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Reproduction studies in male and female rats using atenolol dosages up to 200 mg/kg daily... have not revealed evidence of impaired fertility.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Atenolol has been shown to produce a dose-related increase in embryo/fetal resorptions in rats at doses equal to or greater than 50 mg/kg/day... Although similar effects were not seen in rabbits, the compound was not evaluated in rabbits at doses above 25 mg/kg/day ...

For more Non-Human Toxicity Excerpts (Complete) data for ATENOLOL (6 total), please visit the HSDB record page.

Emergency and supportive measures. 1. Maintain an open airway and assist ventilation if necessary. 2. Treat coma, seizures, hypotension, hyperkalemia, and hypoglycemia if they occur. 3. Treat bradycardia with atropine, ... IV; isoproterenol ... ; or cardiac pacing. 4. Treat bronchospasm with nebulized bronchodilators. 5. Continuously monitor the vital signs and ECG for at least 6 hours after ingestion. /Beta-adrenergic blockers/

Specific drugs and antidotes. 1. Bradycardia and hypotension resistant to... /normal/ measures should be treated with glucagon, ... . Epinephrine (intravenous) infusion ... and titrating to effect. 2. Wide complex conduction defects caused by membrane-depressant poisoning may respond to sodium bicarbonate, ... as given for tricyclic antidepressant overdose. 3. Torsades de pointes polymorphous ventricular tachycardia associated with QT prolongation resulting from sotalol poisoning can be treated with isoproterenol infusion, magnesium, or overdrive pacing. Correction of hypokalemia may also be useful. /Beta-adrenergic blockers/

Decontamination. 1. Prehospital. Administer activated charcoal if available. 2. Hospital. Administer activated charcoal. Consider gastric lavage for large ingestions, especially involving propranolol. Gastric emptying is not necessary for small ingestions if activated charcoal can be given promptly. /Beta-adrenergic blockers/

Enhanced elimination. Most beta blockers, especially the more toxic drugs such as propranolol, are highly lipophilic and have a large volume of distribution (Vd). For those with a relatively small volume of distribution coupled with a long half-life or low intrinsic clearance (eg, acebutolol, atenolol, nadolol, or sotalol), hemoperfusion, hemodialysis, or repeat-dose charcoal may be effective. /Beta-adrenergic blockers/

For more Antidote and Emergency Treatment (Complete) data for ATENOLOL (6 total), please visit the HSDB record page.

Hazard Traits - Developmental Toxicity；Authoritative List - Prop 65；Report - regardless of intended function of ingredient in the product

Atenolol: Does not have an individual approval but may be used under an appropriate group standard

Atenolol, used as a beta adrenergic blocking agent, was approved by FDA for marketing in the United States 8/81.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed drug products, incl atenolol, approved on the basis of safety and effectiveness by FDA under sections 505 and 507 of the Federal Food, Drug, and Cosmetic Act.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

C07AB03

C07AB03

C - Cardiovascular system；C07 - Beta blocking agents；C07A - Beta blocking agents；C07AB - Beta blocking agents, selective；C07AB03 - Atenolol

QC - Cardiovascular system；QC07 - Beta blocking agents；QC07A - Beta blocking agents；QC07AB - Beta blocking agents, selective；QC07AB03 - Atenolol

C07AB03

Atenolol is a cardio-selective beta-blocker and as such exerts most of its effects on the heart. It acts as an antagonist to sympathetic innervation and prevents increases in heart rate, electrical conductivity, and contractility in the heart due to increased release of norepinephrine from the peripheral nervous system. Together the decreases in contractility and rate produce a reduction in cardiac output resulting in a compensatory increase in peripheral vascular resistance in the short-term. This response later declines to baseline with long-term use of atenolol. More importantly, this reduction in the work demanded of the myocardium also reduces oxygen demand which provides therapeutic benefit by reducing the mismatch of oxygen supply and demand in settings where coronary blood flow is limited, such as in coronary atherosclerosis. Reducing oxygen demand, particularly due to exercise, can reduce the frequency of angina pectoris symptoms and potentially improve survival of the remaining myocardium after myocardial infarction. The decrease in rate of sinoatrial node potentials, electrical conduction, slowing of potentials traveling through the atrioventricular node, and reduced frequency of ectopic potentials due to blockade of adrenergic beta receptors has led to benefit in arrhythmic conditions such as atrial fibrillation by controlling the rate of action potential generation and allowing for more effective coordinated contractions. Since a degree of sympathetic activity is necessary to maintain cardiac function, the reduced contractility induced by atenolol may precipitate or worsen heart failure, especially during volume overload. The effects of atenolol on blood pressure have been established, although it is less effective than alternative beta-blockers, but the mechanism has not yet been characterized. As a β1 selective drug, it does not act via the vasodilation produced by non-selective agents. Despite this there is a sustained reduction in peripheral vascul

Atenolol is a cardioselective beta-blocker, called such because it selectively binds to the β1-adrenergic receptor as an antagonist up to a reported 26 fold more than β2 receptors. Selective activity at the β1 receptor produces cardioselectivity due to the higher population of this receptor in cardiac tissue. Some binding to β2 and possibly β3 receptors can still occur at therapeutic dosages but the effects mediated by antagonizing these are significantly reduced from those of non-selective agents. β1 and β2 receptors are G_s coupled therefore antagonism of their activation reduces activity of adenylyl cyclase and its downstream signalling via cyclic adenosime monophosphate and protein kinase A (PKA). In cardiomyocytes PKA is thought to mediate activation of L-type calcium channels and ryanodine receptors through their phosphorylation. L-type calcium channels can then provide an initial rise in intracellular calcium and trigger the ryanodine receptors to release calcium stored in the sarcoplasmic reticulum (SR) and increased contractility. PKA also plays a role in the cessation of contraction by phosphorylating phospholamban which in turn increases the affinity of SR Ca²⁺ ATPase to increase reuptake of calcium into the SR. It also phophorylates troponin I to reduce affinity of the protein for calcium. Both of these events lead to a reduction in contraction which, when coupled with the initial increase in contraction, allows for faster cycling and consequently higher heart rate with increased contractility. L-type calcium channels are also a major contributor to cardiac depolarization and their activation can increase frequency of action potentials and possibly the incidence of ectopic potentials. Similar inihibitory events occur in the bronchial smooth muscle to mediate relaxation including phosphorylation of myosin light-chain kinase, reducing its affinity for calcium. PKA also inhibits the excitatory G_q coupled pathway by phosph

By inhibiting myocardial beta 1-adrenergic receptors, atenolol produces negative chronotropic and inotropic activity. The negative chronotropic action of atenolol on the sinoatrial node results in a decrease in the rate of sinoatrial node discharge and an increase in recovery time, thereby decreasing resting and exercise stimulated heart rate and reflex orthostatic tachycardia by about 25-35%. High doses of the drug may produce sinus arrest, especially in patients with sinoatrial node disease (eg, sick sinus syndrome). Atenolol also slows conduction in the atrioventricular nose. Although stroke index may be increased moderately by about 10%, atenolol usually reduces cardiac output by about 20% probably secondary to its effect on heart rate. The decrease in myocardial contractability and heart rate, as well as the reduction in blood pressure, produced by atenolol generally lead to a reduction in myocardial oxygen consumption which accounts for the effectiveness of the drug in chronic stable angina pectoris; however, atenolol can increase oxygen requirements by increasing left ventricular fiber length and end-diastolic pressure, particularly in patients with cardiac failure.

Atenolol suppresses plasma renin activity and suppresses the renin aldosterone angiotensin system.

The toxic actions of beta-blockers appear to be related to properties such as membrane depressant activity and possibly due to actions on beta-adrenoceptors distinct from those in the cardiovascular system.

6-7 hrs.

In patients with normal renal function, atenolol has a plasma half-life (t1/2) of 6-7 hours. Children with normal renal function may exhibit a shorter elimination half-life. In one study in children ages 5-16 (mean: 8.9) with arhythmias and normal renal and hepatic function, the terminal elimination half-life averaged 4.6 hours. Plasma t1/2 of the drug increases to 16-27 hours in patients with creatinine clearances of 15-35 ml/minute per 1.73 sq m and exceeds 27 hours with progressive renal impairment.

The half-life in the elderly was significantly longer (8.8 + or - 0.9 hr) compared with that in the young (5.8 + or - 1.1 hr) (p < 0.01).

Minimal metabolism in the liver. The sole non-conjugated metabolite is the product of a hydroxylation reaction at the carbon between the amide and benzene groups. The only other metabolite to be confirmed is a glucuronide conjugate. These metabolites make up 5-8% and 2% of the renally excreted dose with 87-90% appearing as unchanged drug. The hydroxylated metabolite is exerts 1/10th the beta-blocking activity of atenolol.

Minimal hepatic metabolism; removable by hemodialysis; very low lipid solubility.

Little or no metabolism of atenolol occurs in the liver. Approximately 40-50% of an oral dose of the drug is excreted in urine unchanged. The remainder is excreted unchanged in feces, principally as unabsorbed drug. About 1-12% of atenolol is reportedly removed by hemodialysis.

Hepatic (minimal) Route of Elimination: Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the feces. Unlike propranolol or metoprolol, but like nadolol, atenolol undergoes little or no metabolism by the liver, and the absorbed portion is eliminated primarily by renal excretion. Half Life: 6-7 hours

50VV3VW0TI

ATENOLOL

Mechanisms of Action [MoA] - Adrenergic beta-Antagonists

Established Pharmacologic Class [EPC] - beta-Adrenergic Blocker

Atenolol is a beta-Adrenergic Blocker. The mechanism of action of atenolol is as an Adrenergic beta-Antagonist.

ATENOLOL

Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.

Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.

Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.

Drugs that bind to and block the activation of ADRENERGIC BETA-1 RECEPTORS.

Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, with the remainder being excreted unchanged in the feces. Administering atenolol with food can decrease the AUC by about 20%. While atenolol can cross the blood-brain barrier, it does so slowly and to a small extent.

85% is eliminated by the kidneys following IV administration with 10% appearing in the feces.

Total Vd of 63.8-112.5 L. Atenolol distributes into a central volume of 12.8-17.5 L along with two peripheral compartments with a combined volume of 51-95 L. Distribution takes about 3 hrs for the central compartment, 4 hrs for the shallower peripheral compartment, and 5-6 hrs for the deeper peripheral compartment.

Total clearance is estimated at 97.3-176.3 mL/min with a renal clearance of 95-168 mL/min.

In animals, atenolol is well distributed into most tissues and fluids except brain and /cerebrospinal fluid/. Unlike propranolol, only a small portion of atenolol is apparently distributed into the CNS.

Approximately 5-15% of atenolol is bound to plasma protein.

MEDICATION

Use (kg) in Switzerland (2009): >1000；Use (kg; approx.) in Germany (2009): >7500；Use (kg; exact) in Germany (2009): 7481；Use (kg) in USA (2002): 41900；Use (kg) in France (2004): 18337；Consumption (g per capita) in Switzerland (2009): 0.13；Consumption (g per capita; approx.) in Germany (2009): 0.092；Consumption (g per capita; exact) in Germany (2009): 0.091；Consumption (g per capita) in the USA (2002): 0.15；Consumption (g per capita) in France (2004): 0.3；Excretion rate: 0.83；Calculated removal (%): 22

For the management of hypertention and long-term management of patients with angina pectoris

Oral tablets, 25 mg, Tenormin (with povidone), AstraZeneca; 50 mg, atenolol tablets, Tenormin (with povidone; scored), AstraZeneca; 100 mg, atenolol tablets, Tenormin (with povidone), AstraZeneca; parenteral injection, for IV use, 0.5 mg/ml Tenormin, AstraZeneca.

Atehexal, Ateno basan, Atenol, Cuxanorm, Ibinolo, Myocord, Prenormine, Seles Beta, Tenoblock, Tenormin, Uniloc

Pharmaceuticals

Pharmaceuticals -> Cardiovascular system -> Beta blockers -> Beta blocking agents, selective