Atenolol was first patented in 1969 and received approval for medical use in 1975, after being developed by the British pharmaceutical company Imperial Chemical Industries (ICI). It was introduced to the market in 1976 under the brand name Tenormin and quickly became one of the most widely used beta-blockers worldwide during the 1980s and 1990s. The development of atenolol followed the ground breaking research of pharmacologist Sir James Black, who, in the late 1950s, earned a Nobel Prize for pioneering the beta-blocker class of drugs.
Atenolol is a prescription drug belonging to the beta-blocker class. As a cardio selective beta-blocker, it specifically targets beta-1 adrenergic receptors in the heart, making it effective for managing various cardiovascular conditions. By blocking the action of the hormone epinephrine (adrenaline), atenolol reduces heart rate, decreases the strength of heart contractions, and lowers blood pressure.
BRAND NAMES
Atenolol is marketed under the brand name Tenormin® in the U.S. and various other regions, as well as under many different names, especially in the Indian market. It is a generic beta-blocker commonly prescribed to treat high blood pressure, angina, and to lower the risk of death following a heart attack.
Tenormin® is the most widely recognized brand name for atenolol, available in the U.S. and several other countries.
MECHANISM OF ACTION
Atenolol is classified as a cardio selective beta-blocker because it selectively binds to β1-adrenergic receptors, showing up to 26 times greater affinity for β1 receptors compared to β2 receptors. This selectivity is due to the higher concentration of β1 receptors in cardiac tissue, which contributes to its cardio selective effects. Although atenolol can still bind to β2 and possibly β3 receptors at therapeutic doses, the antagonistic effects on these receptors are much weaker than those seen with non-selective beta-blockers. Both β1 and β2 receptors are coupled to the Gs protein, so blocking their activation leads to decreased activity of adenylyl cyclase and subsequent downstream signaling through cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA).
PHARMACOKINETICS:
Absorption
Atenolol is quickly but partially absorbed from the gastrointestinal tract, with an oral bioavailability of approximately 50%. After taking an oral dose, peak blood concentrations are typically reached within 2 to 4 hours. The drug is mainly eliminated through the kidneys, with only a minor portion metabolized by the liver. Additionally, food intake can reduce the amount of atenolol absorbed by around 20%.
Distribution
Atenolol's distribution is characterized by its low lipophilicity and minimal protein binding, which limits its ability to cross cell membranes and concentrate in the brain.
Metabolism
Atenolol undergoes minimal metabolism, with about 95% of the drug remaining unchanged in the body. Unlike many other beta-blockers, it is not primarily broken down by the liver. The main pathway for its elimination is direct excretion by the kidneys.
Excretion
Atenolol is excreted primarily by the kidneys, with the elimination process largely dependent on renal function. Unlike many other drugs, atenolol undergoes minimal metabolism by the liver before excretion.
PHARMACODYNAMICS
Atenolol is a cardio selective beta-blocker, meaning it primarily affects the heart. It acts as an antagonist to sympathetic nervous system signals, preventing increases in heart rate, electrical conduction, and contractility that are normally triggered by norepinephrine released from the peripheral nervous system. The combined reduction in heart rate and contractility leads to a decrease in cardiac output, which initially causes a compensatory rise in peripheral vascular resistance.
ADMINISTRATION
Atenolol is given either orally in tablet form or through intravenous (IV) injection, depending on the patient's medical needs. Ensuring proper administration—such as taking the medication at consistent times and gradually discontinuing use—is essential for its effectiveness and safety.
DOSAGE AND STRENGTH
Atenolol is an oral beta-blocker available in tablet strengths of 25 mg, 50 mg, and 100 mg. An intravenous injection form is also available, typically for use immediately after a heart attack.
The dosage of atenolol varies depending on the medical condition it is being used to treat.
DRUG INTERACTIONS
Atenolol interacts with many drugs, especially those that influence heart rate and blood pressure, as well as certain supplements and foods. Some interactions may lead to excessively low blood pressure or an abnormally slow heart rate, while others can diminish the effectiveness of atenolol.
FOOD INTERACTIONS
Food interactions with atenolol primarily affect its absorption and effectiveness. While the drug can be taken with or without food, consistency is important. Certain foods and supplements have more notable interactions and should be discussed with a doctor.
CONTRAINDICATIONS
Atenolol, a beta-blocker, is not recommended for patients with severe heart conditions or certain other medical issues that may be aggravated by its use. It is also contraindicated in individuals who have a known allergy or hypersensitivity to atenolol or any of its ingredients.
SIDE EFFECTS
Blurred vision
Chest tightness
Cold hands or feet
Confusion
Difficulty or labored breathing
Dizziness, faintness, or light-headedness upon suddenly standing up from a sitting or lying position
Excessive sweating
TOXICITY
The toxicity of atenolol, a beta-blocker, mainly occurs in cases of overdose, which can critically affect the cardiovascular system and carries a significant risk of fatality. Although atenolol is usually cardio selective at therapeutic doses, an overdose results in non-selective beta-blockade, causing severe bradycardia (slow heart rate) and hypotension (low blood pressure).
