| Indication | For the management of hypertention and long-term management of patients with angina pectoris |
| Pharmacodynamics | Atenolol, a competitive beta(1)-selective adrenergic antagonist, has the lowest lipid solubility of this drug class. Although it is similar to metoprolol, atenolol differs from pindolol and propranolol in that it does not have intrinsic sympathomimetic properties or membrane-stabilizing activity. Atenolol is used alone or with chlorthalidone in the management of hypertension and edema. |
| Mechanism of action | 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. |
| Absorption | Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the feces. |
| Volume of distribution | Not Available |
| Protein binding | Plasma protein binding is 6-16% |
| Metabolism | 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 |
| Clearance | Not Available |
| Toxicity | LD50=2000-3000 mg/kg(orally in mice). Symptoms of an atenolol overdose include a slow heart beat, shortness of breath, fainting, dizziness, weakness, confusion, nausea, and vomiting. |