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Atenolol
TENORMIN ® FDA Package Insert
Indications and Usage
Dosage and Administration
Contraindications
Warnings and Precautions
Adverse Reactions
Drug Interactions
Use in Specific Populations
Overdosage
Description
Clinical Pharmacology
Nonclinical Toxicology
How Supplied/Storage and Handling
Labels and Packages
Clinical Trials on Atenolol
ClinicalTrials.gov

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sheng Shi, M.D. [2]

For patient information about Atenolol, click here.

Synonyms / Brand Names: TENORMIN®

Overview

Atenolol is a selective β1 receptor antagonist, a drug belonging to the group of beta blockers (sometimes written β-blockers), a class of drugs used primarily in cardiovascular diseases. Introduced in 1976, atenolol was developed as a replacement for propranolol in the treatment of hypertension. The chemical works by slowing down the heart and reducing its workload. Unlike propranolol, atenolol does not pass through the blood–brain barrier thus avoiding various central nervous system side effects.[1]

Atenolol is one of the most widely used β-blockers in the United Kingdom and was once the first-line treatment for hypertension. The role for β-blockers in hypertension was downgraded in June 2006 in the United Kingdom to fourth-line, as they perform less appropriately or effectively than newer drugs, particularly in the elderly.

Category

Beta blockers

FDA Package Insert

TENORMIN (atenolol) tablet

Indications and Usage | Dosage and Administration | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Use in Specific Populations | Overdosage | Description | Clinical Pharmacology | Nonclinical Toxicology | How Supplied/Storage and Handling | Labels and Packages

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Mechanism of Action

The mechanisms of the antihypertensive effects of beta-blocking agents have not been established. Several possible mechanisms have been proposed and include: (1) competitive antagonism of catecholamines at peripheral (especially cardiac) adrenergic neuron sites, leading to decreased cardiac output, (2) a central effect leading to reduced sympathetic outflow to the periphery, and (3) suppression of renin activity.

References

  1. ↑ Agon P, Goethals P, Van Haver D, Kaufman JM (August 1991). "Permeability of the blood–brain barrier for atenolol studied by positron emission tomography". J. Pharm. Pharmacol. 43 (8): 597–600. doi:10.1111/j.2042-7158.1991.tb03545.x. PMID 1681079.
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