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Details

Stereochemistry RACEMIC
Molecular Formula C14H22N2O3.ClH
Molecular Weight 302.797
Optical Activity ( + / - )
Defined Stereocenters 0 / 1
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of ATENOLOL HYDROCHLORIDE

SMILES

Cl.CC(C)NCC(O)COC1=CC=C(CC(N)=O)C=C1

InChI

InChIKey=FFDDLJYKJQGSPW-UHFFFAOYSA-N
InChI=1S/C14H22N2O3.ClH/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18;/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18);1H

HIDE SMILES / InChI

Description
Curator's Comment: description was created based on several sources, including http://www.world-medicinehistory.com/2014/08/discovery-of-atenolol.html https://www.ncbi.nlm.nih.gov/pubmed/3730023

Atenolol is a Beta-1 cardio-selective adreno-receptor blocking agent discovered and developed by ICI in 1976. Atenolol was launched in the market under the trade name Tenormin in 1976, and became the best-selling Beta-blocker in the world in the 1980s and 1990s. TENORMIN is indicated for the treatment of hypertension, to lower blood pressure; also for the long-term management of patients with angina pectoris and also is indicated in the management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality. 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. Hypotensive mechanism of atenolol is very complex. Decrease in CO and inhibition of renin-angiotensin-aldosterone system may mainly be responsible for hypotension. It is likely that potassium retaining action of atenolol partly contributes to its hypotensive action. It is also hypothetized that renal kallikrein-kinin system may play a role in modulating the hypotensive action of atenolol.

CNS Activity

Curator's Comment: Known to be CNS non penetrant in dog. Human data not available.

Approval Year

Targets

Targets

Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
TENORMIN

Approved Use

Hypertension Atenolol tablets are indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure lowers the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including atenolol tablets. Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise and limited sodium intake. Many patients will require more than one drug to achieve blood pressure goals. For specific advice on goals and management, see published guidelines, such as those of the National High Blood Pressure Education Program’s Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC). Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits. The largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly. Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit. Relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension (for example, patients with diabetes or hyperlipidemia), and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal. Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black patients, and many antihypertensive drugs have additional approved indications and effects (e.g., on angina, heart failure or diabetic kidney disease). These considerations may guide selection of therapy. Atenolol tablets may be administered with other antihypertensive agents. Angina Pectoris Due to Coronary Atherosclerosis Atenolol tablets are indicated for the long-term management of patients with angina pectoris. Acute Myocardial Infarction Atenolol tablets are indicated in the management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality. Treatment can be initiated as soon as the patient's clinical condition allows. (See DOSAGE AND ADMINISTRATION, CONTRAINDICATIONS, and WARNINGS.) In general, there is no basis for treating patients like those who were excluded from the ISIS-1 trial (blood pressure less than 100 mm Hg systolic, heart rate less than 50 bpm) or have other reasons to avoid beta blockade. As noted above, some subgroups (e.g., elderly patients with systolic blood pressure below 120 mm Hg) seemed less likely to benefit.

Launch Date

1981
Primary
TENORMIN

Approved Use

Hypertension Atenolol tablets are indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure lowers the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including atenolol tablets. Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise and limited sodium intake. Many patients will require more than one drug to achieve blood pressure goals. For specific advice on goals and management, see published guidelines, such as those of the National High Blood Pressure Education Program’s Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC). Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits. The largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly. Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit. Relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension (for example, patients with diabetes or hyperlipidemia), and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal. Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black patients, and many antihypertensive drugs have additional approved indications and effects (e.g., on angina, heart failure or diabetic kidney disease). These considerations may guide selection of therapy. Atenolol tablets may be administered with other antihypertensive agents. Angina Pectoris Due to Coronary Atherosclerosis Atenolol tablets are indicated for the long-term management of patients with angina pectoris. Acute Myocardial Infarction Atenolol tablets are indicated in the management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality. Treatment can be initiated as soon as the patient's clinical condition allows. (See DOSAGE AND ADMINISTRATION, CONTRAINDICATIONS, and WARNINGS.) In general, there is no basis for treating patients like those who were excluded from the ISIS-1 trial (blood pressure less than 100 mm Hg systolic, heart rate less than 50 bpm) or have other reasons to avoid beta blockade. As noted above, some subgroups (e.g., elderly patients with systolic blood pressure below 120 mm Hg) seemed less likely to benefit.

Launch Date

1981
Primary
TENORMIN

Approved Use

Hypertension Atenolol tablets are indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure lowers the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including atenolol tablets. Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise and limited sodium intake. Many patients will require more than one drug to achieve blood pressure goals. For specific advice on goals and management, see published guidelines, such as those of the National High Blood Pressure Education Program’s Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC). Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits. The largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly. Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit. Relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension (for example, patients with diabetes or hyperlipidemia), and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal. Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black patients, and many antihypertensive drugs have additional approved indications and effects (e.g., on angina, heart failure or diabetic kidney disease). These considerations may guide selection of therapy. Atenolol tablets may be administered with other antihypertensive agents. Angina Pectoris Due to Coronary Atherosclerosis Atenolol tablets are indicated for the long-term management of patients with angina pectoris. Acute Myocardial Infarction Atenolol tablets are indicated in the management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality. Treatment can be initiated as soon as the patient's clinical condition allows. (See DOSAGE AND ADMINISTRATION, CONTRAINDICATIONS, and WARNINGS.) In general, there is no basis for treating patients like those who were excluded from the ISIS-1 trial (blood pressure less than 100 mm Hg systolic, heart rate less than 50 bpm) or have other reasons to avoid beta blockade. As noted above, some subgroups (e.g., elderly patients with systolic blood pressure below 120 mm Hg) seemed less likely to benefit.

Launch Date

1981
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
1.75 μg/mL
200 mg single, oral
dose: 200 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
ATENOLOL plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
0.75 μg/mL
100 mg single, oral
dose: 100 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
ATENOLOL plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
AUC

AUC

ValueDoseCo-administeredAnalytePopulation
0.3 μg × h/mL
10 mg single, intravenous
dose: 10 mg
route of administration: Intravenous
experiment type: SINGLE
co-administered:
ATENOLOL plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
13.45 μg × h/mL
200 mg single, oral
dose: 200 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
ATENOLOL plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
8.47 μg × h/mL
100 mg single, oral
dose: 100 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
ATENOLOL plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
T1/2

T1/2

ValueDoseCo-administeredAnalytePopulation
5.4 h
200 mg single, oral
dose: 200 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
ATENOLOL plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
5.9 h
100 mg single, oral
dose: 100 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
ATENOLOL plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
7 h
unknown
ATENOLOL plasma
Homo sapiens
population: UNKNOWN
age: UNKNOWN
sex: UNKNOWN
food status: UNKNOWN
Funbound

Funbound

ValueDoseCo-administeredAnalytePopulation
94%
unknown
ATENOLOL plasma
Homo sapiens
population: UNKNOWN
age: UNKNOWN
sex: UNKNOWN
food status: UNKNOWN
Doses

Doses

DosePopulationAdverse events​
540 mg 1 times / day multiple, oral (mean)
Studied dose
Dose: 540 mg, 1 times / day
Route: oral
Route: multiple
Dose: 540 mg, 1 times / day
Sources:
unhealthy, 42 to 65 years
n = 16
Health Status: unhealthy
Condition: hypertension
Age Group: 42 to 65 years
Sex: M+F
Population Size: 16
Sources:
DLT: Bradycardia...
Dose limiting toxicities:
Bradycardia (31%)
Sources:
900 mg 1 times / day multiple, oral
Highest studied dose
Dose: 900 mg, 1 times / day
Route: oral
Route: multiple
Dose: 900 mg, 1 times / day
Sources:
unhealthy, 42 years
n = 1
Health Status: unhealthy
Condition: hypertension
Age Group: 42 years
Sex: M
Population Size: 1
Sources:
Other AEs: Somnolence, Exertional dyspnea...
Other AEs:
Somnolence
Exertional dyspnea
Sources:
150 mg 1 times / day multiple, oral (mean)
Studied dose
Dose: 150 mg, 1 times / day
Route: oral
Route: multiple
Dose: 150 mg, 1 times / day
Sources:
unhealthy, mean age 53 years
n = 9
Health Status: unhealthy
Condition: angina pectoris
Age Group: mean age 53 years
Sex: M+F
Population Size: 9
Sources:
DLT: Fatigue...
Dose limiting toxicities:
Fatigue (11%)
Sources:
100 mg 1 times / day multiple, oral
Recommended
Dose: 100 mg, 1 times / day
Route: oral
Route: multiple
Dose: 100 mg, 1 times / day
Sources:
unhealthy, mean age 62 years
n = 32
Health Status: unhealthy
Condition: ventricular ectopy
Age Group: mean age 62 years
Sex: M+F
Population Size: 32
Sources:
Disc. AE: Vertigo, Bronchospasm...
AEs leading to
discontinuation/dose reduction:
Vertigo (6.2%)
Bronchospasm (3%)
Fatigue (3%)
Sources:
50 mg 1 times / day multiple, oral
Recommended
Dose: 50 mg, 1 times / day
Route: oral
Route: multiple
Dose: 50 mg, 1 times / day
Sources:
unhealthy, mean age 62 years
n = 32
Health Status: unhealthy
Condition: ventricular ectopy
Age Group: mean age 62 years
Sex: M+F
Population Size: 32
Sources:
Disc. AE: Ventricular tachycardia...
AEs leading to
discontinuation/dose reduction:
Ventricular tachycardia (3%)
Sources:
50 mg 1 times / day steady, oral
Dose: 50 mg, 1 times / day
Route: oral
Route: steady
Dose: 50 mg, 1 times / day
Sources:
unhealthy
n = 18
Health Status: unhealthy
Condition: Hypertension
Population Size: 18
Sources:
Other AEs: Fatigue, Nausea...
Other AEs:
Fatigue (below serious, 2 patients)
Nausea (below serious, 2 patients)
Sources:
AEs

AEs

AESignificanceDosePopulation
Bradycardia 31%
DLT
540 mg 1 times / day multiple, oral (mean)
Studied dose
Dose: 540 mg, 1 times / day
Route: oral
Route: multiple
Dose: 540 mg, 1 times / day
Sources:
unhealthy, 42 to 65 years
n = 16
Health Status: unhealthy
Condition: hypertension
Age Group: 42 to 65 years
Sex: M+F
Population Size: 16
Sources:
Exertional dyspnea
900 mg 1 times / day multiple, oral
Highest studied dose
Dose: 900 mg, 1 times / day
Route: oral
Route: multiple
Dose: 900 mg, 1 times / day
Sources:
unhealthy, 42 years
n = 1
Health Status: unhealthy
Condition: hypertension
Age Group: 42 years
Sex: M
Population Size: 1
Sources:
Somnolence
900 mg 1 times / day multiple, oral
Highest studied dose
Dose: 900 mg, 1 times / day
Route: oral
Route: multiple
Dose: 900 mg, 1 times / day
Sources:
unhealthy, 42 years
n = 1
Health Status: unhealthy
Condition: hypertension
Age Group: 42 years
Sex: M
Population Size: 1
Sources:
Fatigue 11%
DLT
150 mg 1 times / day multiple, oral (mean)
Studied dose
Dose: 150 mg, 1 times / day
Route: oral
Route: multiple
Dose: 150 mg, 1 times / day
Sources:
unhealthy, mean age 53 years
n = 9
Health Status: unhealthy
Condition: angina pectoris
Age Group: mean age 53 years
Sex: M+F
Population Size: 9
Sources:
Bronchospasm 3%
Disc. AE
100 mg 1 times / day multiple, oral
Recommended
Dose: 100 mg, 1 times / day
Route: oral
Route: multiple
Dose: 100 mg, 1 times / day
Sources:
unhealthy, mean age 62 years
n = 32
Health Status: unhealthy
Condition: ventricular ectopy
Age Group: mean age 62 years
Sex: M+F
Population Size: 32
Sources:
Fatigue 3%
Disc. AE
100 mg 1 times / day multiple, oral
Recommended
Dose: 100 mg, 1 times / day
Route: oral
Route: multiple
Dose: 100 mg, 1 times / day
Sources:
unhealthy, mean age 62 years
n = 32
Health Status: unhealthy
Condition: ventricular ectopy
Age Group: mean age 62 years
Sex: M+F
Population Size: 32
Sources:
Vertigo 6.2%
Disc. AE
100 mg 1 times / day multiple, oral
Recommended
Dose: 100 mg, 1 times / day
Route: oral
Route: multiple
Dose: 100 mg, 1 times / day
Sources:
unhealthy, mean age 62 years
n = 32
Health Status: unhealthy
Condition: ventricular ectopy
Age Group: mean age 62 years
Sex: M+F
Population Size: 32
Sources:
Ventricular tachycardia 3%
Disc. AE
50 mg 1 times / day multiple, oral
Recommended
Dose: 50 mg, 1 times / day
Route: oral
Route: multiple
Dose: 50 mg, 1 times / day
Sources:
unhealthy, mean age 62 years
n = 32
Health Status: unhealthy
Condition: ventricular ectopy
Age Group: mean age 62 years
Sex: M+F
Population Size: 32
Sources:
Fatigue below serious, 2 patients
50 mg 1 times / day steady, oral
Dose: 50 mg, 1 times / day
Route: oral
Route: steady
Dose: 50 mg, 1 times / day
Sources:
unhealthy
n = 18
Health Status: unhealthy
Condition: Hypertension
Population Size: 18
Sources:
Nausea below serious, 2 patients
50 mg 1 times / day steady, oral
Dose: 50 mg, 1 times / day
Route: oral
Route: steady
Dose: 50 mg, 1 times / day
Sources:
unhealthy
n = 18
Health Status: unhealthy
Condition: Hypertension
Population Size: 18
Sources:
PubMed

PubMed

TitleDatePubMed
L-Dopa uptake and dopamine production in proximal tubular cells are regulated by beta(2)-adrenergic receptors.
2000 Jul
[A possible adverse effect from the association of losartan-mefenamic acid in hemodialysis].
2001
Effect of strict blood pressure control on proteinuria in renal patients treated with different antihypertensive drugs.
2001
[Postinfarction remodeling of the left atrium and left ventricle: effects of long-term treatment with beta adrenergic blockers and angiotensin converting enzyme inhibitors].
2001
The effects of opioids on isolated human pregnant uterine muscles.
2001 Apr
Mass spectrometric quantitation of chiral drugs by the kinetic method.
2001 Apr 15
Small blood volumes from children for quantitative sotalol determination using high-performance liquid chromatography.
2001 Apr 5
Quantitative structure-retention and retention-activity relationships of beta-blocking agents by micellar liquid chromatography.
2001 Apr 6
Use of vancomycin silica stationary phase in packed capillary electrochromatography I. Enantiomer separation of basic compounds.
2001 Feb
Lack of efficacy of atenolol for the prevention of neurally mediated syncope in a highly symptomatic population: a prospective, double-blind, randomized and placebo-controlled study.
2001 Feb
Involvement of both G protein alphas and beta gamma subunits in beta-adrenergic stimulation of vascular L-type Ca(2+) channels.
2001 Feb
Reversal of deteriorated fractal behavior of heart rate variability by beta-blocker therapy in patients with advanced congestive heart failure.
2001 Jan
A N-terminal PTHrP peptide fragment void of a PTH/PTHrP-receptor binding domain activates cardiac ET(A) receptors.
2001 Jan
Antihypertensive monotherapy and cardiovascular responses to an acoustic startle stimulus.
2001 Jan
Catecholaminergic regulation of Na-K-Cl cotransport in pigmented ciliary epithelium: differences between PE and NPE.
2001 Jan
Activation of sympathoadrenomedullary system increases pulmonary nitric oxide production in the rabbit.
2001 Jan 12
Amantadine-induced cortical myoclonus.
2001 Jan 23
Chiral ion-pair chromatography on porous graphitized carbon using N-blocked dipeptides as counter ions.
2001 Jan 5
Role of alpha1-blockade in congenital long QT syndrome: investigation by exercise stress test.
2001 Jul
A new aspect of view in synthesizing new type beta-adrenoceptor blockers with ancillary antioxidant activities.
2001 Jul
Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope: a multicenter, randomized, controlled trial.
2001 Jul 3
Pharmacoutilization of antihypertensive drugs: a model of analysis.
2001 Jun
Pharmacological investigation on nigrescigenin-a cardenolide from Parquetina nigrescens (Afzel.) Bullock: comparative studies on cardiotonic effects of Parquetina nigrescens, g-strophanthin and noradrenaline in guinea-pig isolated atria.
2001 Jun
Usefulness of the head-upright tilt test for distinguishing syncope and epilepsy in children.
2001 Jun
Regression of left ventricular hypertrophy in human hypertension with irbesartan.
2001 Jun
Rationale, design, methods and baseline demography of participants of the Anglo-Scandinavian Cardiac Outcomes Trial. ASCOT investigators.
2001 Jun
[Panniculitis induced by MINE chemotherapy].
2001 Jun-Jul
Characterization of [3H]CGP 12177 binding to beta-adrenergic receptors in intact eel hepatocytes.
2001 Mar
Structure-hepatic disposition relationships for cationic drugs in isolated perfused rat livers: transmembrane exchange and cytoplasmic binding process.
2001 May
Stereospecific pharmacokinetics and pharmacodynamics of beta-adrenergic blockers in humans.
2001 May-Aug
A prospective comparison of four antihypertensive agents in daily clinical practice.
2001 May-Jun
Patents

Sample Use Guides

Hypertension: The initial dose of TENORMIN (atenolol) is 50 mg given as one tablet a day either alone or added to diuretic therapy. The full effect of this dose will usually be seen within one to two weeks. Angina Pectoris: The initial dose of TENORMIN is 50 mg given as one tablet a day. If an optimal response is not achieved within one week, the dosage should be increased to TENORMIN 100 mg given as one tablet a day. In patients with definite or suspected acute myocardial infarction, treatment with TENORMIN I.V. Treatment should begin with the intravenous administration of 5 mg TENORMIN over 5 minutes followed by another 5 mg intravenous injection 10 minutes later. TENORMIN I.V. Injection should be administered under carefully controlled conditions including monitoring of blood pressure, heart rate, and electrocardiogram.
Route of Administration: Other
The aim of the study was to assess the effects of the beta-blocker atenolol and the high energy demand in an ischaemia-reperfusion model free of neurohormonal and vascular factors. There was exposed Langendorff-perfused isolated rat hearts to low-flow ischaemia (30 min) and reflow (20 min). Three groups of hearts were used: control hearts (n =11), hearts that were perfused with 2.5 micrograms l-1atenolol (n =9), and hearts electrically paced during ischaemia to distinguish the effect of heart rate from that of the drug (n =9). During ischaemia, the pressure-rate product was 2.3+/-0.2, 5.2+/-1.1, and 3.3+/-0.3 mm Hg 10(3) min in the control, atenolol and paced hearts, respectively. In addition, the ATP turnover rate, calculated from venous (lactate), oxygen uptake and flow, was higher in atenolol (11.2+/-1.7 micromol min-1) and paced (8.1+/-0.8 micromol min-1) hearts than in control (6.2+/-0.8 micromol min-1). At the end of reflow, the pressurexrate product recovered 75.1+/-6.4% of baseline in control vs 54.1+/-9.1 and 48.8+/-4.4% in atenolol and paced hearts (P<0.05).
Name Type Language
ATENOLOL HYDROCHLORIDE
WHO-DD  
Common Name English
4-(2-HYDROXY-3-((ISOPROPYL)AMINO)PROPOXY)PHENYLACETAMIDE HYDROCHLORIDE
Systematic Name English
ATENOLOL HCL
Common Name English
Atenolol hydrochloride [WHO-DD]
Common Name English
Code System Code Type Description
PUBCHEM
119274
Created by admin on Fri Dec 15 17:15:09 GMT 2023 , Edited by admin on Fri Dec 15 17:15:09 GMT 2023
PRIMARY
EPA CompTox
DTXSID4020111
Created by admin on Fri Dec 15 17:15:09 GMT 2023 , Edited by admin on Fri Dec 15 17:15:09 GMT 2023
PRIMARY
EVMPD
SUB00615MIG
Created by admin on Fri Dec 15 17:15:09 GMT 2023 , Edited by admin on Fri Dec 15 17:15:09 GMT 2023
PRIMARY
SMS_ID
100000089975
Created by admin on Fri Dec 15 17:15:09 GMT 2023 , Edited by admin on Fri Dec 15 17:15:09 GMT 2023
PRIMARY
FDA UNII
6DI0UT7U1Q
Created by admin on Fri Dec 15 17:15:09 GMT 2023 , Edited by admin on Fri Dec 15 17:15:09 GMT 2023
PRIMARY
CAS
51706-40-2
Created by admin on Fri Dec 15 17:15:09 GMT 2023 , Edited by admin on Fri Dec 15 17:15:09 GMT 2023
PRIMARY
ECHA (EC/EINECS)
257-355-1
Created by admin on Fri Dec 15 17:15:09 GMT 2023 , Edited by admin on Fri Dec 15 17:15:09 GMT 2023
PRIMARY