Atenolol !
A β1-selective beta blocker cleared by the kidneys. Used for high blood pressure, angina and after a heart attack.
Updated 2026-11-01
The figure shows the turkey β1 receptor with cyanopindolol, another beta blocker in the same binding site where atenolol acts; no structure with atenolol bound is available.
Mechanism of action
Atenolol blocks β1 receptors in the heart and the kidney's juxtaglomerular cells. Heart rate, contractility and renin release fall, so oxygen demand and blood pressure fall. It is water-soluble: it barely enters the brain, is hardly metabolised and is excreted unchanged by the kidneys. Its β1 selectivity is relative and fades at higher exposure.
- Atenolol blocks cardiac and renal β1 receptors
- Heart rate and contractility fall; less renin is released
- Myocardial oxygen demand and blood pressure fall
Pharmacokinetics
- Absorption
- Only part of an oral dose is absorbed
- Metabolism
- Little or no liver metabolism
- Elimination
- Excreted mainly unchanged by the kidneys, so it accumulates in kidney failure
- Half-life
- About 6 to 7 hours by mouth
Indications
- High blood pressure Arterial hypertension →
- Chronic angina from coronary atherosclerosis Stable angina →
- Acute myocardial infarction in stable patients Myocardial Infarction (Heart Attack) →
Adverse effects
Common
- Bradycardia
- Fatigue and cold hands and feet
- Dizziness and low blood pressure
- Masked signs of hypoglycaemia (tremor, palpitations)
Contraindications
- Sinus bradycardia
- Heart block greater than first degree
- Cardiogenic shock
- Overt heart failure
Key interactions
- Verapamil or diltiazem
- Added bradycardia, AV block and depressed contractility
- Clonidine
- Worse rebound hypertension when clonidine is stopped; the beta blocker is withdrawn first
- Insulin and oral antidiabetics
- Hypoglycaemia is harder to notice
What is monitored
- Heart rate and blood pressure
- Kidney function
- Signs of heart failure
- Glucose in diabetes
Administration and safety
- Given by mouth; dosing is adjusted in kidney failure because it is cleared by the kidneys
- Never stopped suddenly: it is withdrawn gradually, with limited physical activity meanwhile
- Many «-olol» names look alike: the name is checked on every order
Nursing care
- Check apical pulse and blood pressure before each dose; report bradycardia or hypotension
- Watch for wheezing, breathlessness, oedema or weight gain
- In diabetes, teach that sweating may be the only warning sign of hypoglycaemia
- Teach the patient not to stop it abruptly
Pregnancy and breastfeeding
Atenolol crosses the placenta and, from the second trimester, has been linked to small-for-gestational-age babies; newborns may have bradycardia and hypoglycaemia.
Test yourself
Think of the answer, then tap the question to see it.
How is atenolol eliminated, and what does that mean in kidney failure?
Mostly unchanged by the kidneys, so it accumulates when kidney function is poor and the dosing is adjusted.
Why should atenolol not be stopped suddenly in a patient with angina?
Sudden withdrawal can worsen angina and trigger infarction or ventricular arrhythmias; it is tapered.
Why does atenolol cause fewer central effects (nightmares, depression) than propranolol?
It is water-soluble and crosses the blood-brain barrier poorly, while propranolol is lipid-soluble.
Related drugs
Related conditions
← Back to the class: Beta blockers
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: DailyMed - ATENOLOL tablet (DailyMed (U.S. National Library of Medicine), 2026); ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026).
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Representative model, for educational purposes only.