| 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)
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
Originator
Approval Year
Doses
AEs
Sourcing
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).
ACTIVE MOIETY
SUBSTANCE RECORD
