Details
| Stereochemistry | RACEMIC |
| Molecular Formula | C14H22N2O3.C4H6O4 |
| Molecular Weight | 384.4241 |
| Optical Activity | ( + / - ) |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
OC(=O)CCC(O)=O.CC(C)NCC(O)COC1=CC=C(CC(N)=O)C=C1
InChI
InChIKey=ZKORHZFKCQJATE-UHFFFAOYSA-N
InChI=1S/C14H22N2O3.C4H6O4/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18;5-3(6)1-2-4(7)8/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18);1-2H2,(H,5,6)(H,7,8)
DescriptionCurator'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
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.
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
Target ID: CHEMBL210 |
|||
Target ID: CHEMBL213 |
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
| Primary | TENORMIN Approved UseHypertension 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 Date1981 |
|||
| Primary | TENORMIN Approved UseHypertension 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 Date1981 |
|||
| Primary | TENORMIN Approved UseHypertension 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 Date1981 |
Cmax
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
1.75 μg/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/658112/ |
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 EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/658112/ |
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
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
0.3 μg × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/658112/ |
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 EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/658112/ |
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 EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/658112/ |
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
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
5.4 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/658112/ |
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 EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/658112/ |
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
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
94% |
unknown |
ATENOLOL plasma | Homo sapiens population: UNKNOWN age: UNKNOWN sex: UNKNOWN food status: UNKNOWN |
Doses
| Dose | Population | Adverse 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... |
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... |
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... |
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%) Sources: Bronchospasm (3%) Fatigue (3%) |
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) Sources: Nausea (below serious, 2 patients) |
AEs
| AE | Significance | Dose | Population |
|---|---|---|---|
| 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: |
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
Drug as perpetrator
| Target | Modality | Activity | Metabolite | Clinical evidence |
|---|---|---|---|---|
| weak |
Drug as victim
| Target | Modality | Activity | Metabolite | Clinical evidence |
|---|---|---|---|---|
| no | ||||
| no | ||||
| no | ||||
| yes | ||||
| yes | ||||
| yes | ||||
| yes |
Tox targets
| Target | Modality | Activity | Metabolite | Clinical evidence |
|---|---|---|---|---|
PubMed
| Title | Date | PubMed |
|---|---|---|
| Cardiovascular and adrenergic effects of cigarette smoking during immediate non-selective and selective beta adrenoceptor blockade in humans. | 1979 Jun |
|
| Perindopril/indapamide 2/0.625 mg/day: a review of its place in the management of hypertension. | 2001 |
|
| [Two complex suicidal poisonings with drugs and their medicolegal aspects]. | 2001 |
|
| Barnidipine. | 2001 |
|
| Mechanism of action of noradrenaline on secretion of progesterone and oxytocin by the bovine corpus luteum in vitro. | 2001 |
|
| [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 |
|
| Treating hypertension in women of child-bearing age and during pregnancy. | 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 |
|
| [Efficacy of oncologic surgery. Does anesthesia influence the postoperative outcome?]. | 2001 Apr |
|
| Beta-blockade with nebivolol enhances the acetylcholine-induced cutaneous vasodilation. | 2001 Apr |
|
| ['Licorice hypertension' also caused by licorice tea]. | 2001 Apr 14 |
|
| 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 |
|
| LIFE study--still-blinded results show promise. | 2001 Apr-May |
|
| A 39-year-old man with an overdose of beta-blockers. | 2001 Aug |
|
| Antihypertensive therapy and the risk of malignancies. | 2001 Aug |
|
| Beta2-adrenoceptor-mediated prejunctional facilitation and postjunctional inhibition of sympathetic neuroeffector transmission in the guinea pig vas deferens. | 2001 Aug |
|
| Differential role of adrenoceptors in control of plasma glucose and fatty acids in carp, Cyprinus carpio (L.). | 2001 Aug |
|
| [Intense muscle fatigue: an undesirable effect of beta blockers use in morbid obesity]. | 2001 Feb 24 |
|
| Enhancer aided in vitro permeation of atenolol and prazosin hydrochloride through mice skin. | 2001 Jan |
|
| Antihypertensive effect of alpha- and beta-adrenergic blockade in obese and lean hypertensive subjects. | 2001 Jul |
|
| Effects of drug therapy on cardiac arrhythmias and ischemia in hypertensives with LVH. | 2001 Jul |
|
| Role of alpha1-blockade in congenital long QT syndrome: investigation by exercise stress test. | 2001 Jul |
|
| Influence of atenolol on the kinetics of RT interval rate adaptation in conscious dogs. | 2001 Jul |
|
| A new aspect of view in synthesizing new type beta-adrenoceptor blockers with ancillary antioxidant activities. | 2001 Jul |
|
| Ouabain-induced coronary vasoconstriction in cats is not neurally mediated. | 2001 Jul |
|
| Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope: a multicenter, randomized, controlled trial. | 2001 Jul 3 |
|
| An economic evaluation of atenolol vs. captopril in patients with Type 2 diabetes (UKPDS 54). | 2001 Jun |
|
| Relative efficacy of an angiotensin II antagonist compared with other antihypertensive agents. Olmesartan medoxomil versus antihypertensives. | 2001 Jun |
|
| 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 |
|
| Cardioprotective effect of propranolol from alcohol-induced heart muscle damage as assessed by plasma cardiac troponin-t. | 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 |
|
| Differential effects of nifedipine and co-amilozide on the progression of early carotid wall changes. | 2001 Jun 19 |
|
| [Panniculitis induced by MINE chemotherapy]. | 2001 Jun-Jul |
|
| The release of the substrate for xanthine oxidase in hypertensive patients was suppressed by angiotensin converting enzyme inhibitors and alpha1-blockers. | 2001 Mar |
|
| Progressive intracranial vascular disease with strokes and seizures in a boy with progeria. | 2001 Mar |
|
| Partition coefficients of beta-blockers in bile salt/lecithin micelles as a tool to assess the role of mixed micelles in gastrointestinal absorption. | 2001 Mar 15 |
|
| Smoothed pseudo Wigner-Ville distribution as an alternative to Fourier transform in rats. | 2001 Mar 23 |
|
| Nebivolol and airway responsiveness in the rabbit. | 2001 Mar 23 |
|
| [Concurrent long QT and Brugada syndrome in a single patient]. | 2001 May |
|
| Blood pressure, heart rate, and behavioral responses to psychological "novelty" stress in freely moving rats. | 2001 May |
|
| beta(1)- and beta(2)-Adrenoceptor-mediated thermogenesis and lipid utilization in obese and lean men. | 2001 May |
|
| Determination of the beta-blocker atenolol in plasma by capillary zone electrophoresis. | 2001 May 4 |
|
| 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 |
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).
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Common Name | English |
| Code System | Code | Type | Description | ||
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U5428DG3V4
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136259-69-3
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164512872
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ACTIVE MOIETY
SUBSTANCE RECORD
