Atenolol

Question 1

Drug class?

Answer 1

Beta-blocker

Question 2

How does it work?

Answer 2

Block β1 receptors (adrenoreceptors acting on heart and intestinal smooth muscle – β-receptors in heart are excitatory, usually the opposite). Results in reduced contractility of the heart and reduced cardiac output.

Question 3

Indications?

Answer 3

Hypertension, angina, arrhythmias, migraine prophylaxis.

Question 4

Contra-indications?

Answer 4

Asthma, uncontrolled heart failure, Prinzmetal’s angina, marked bradycardia, hypotension, sick sinus syndrome, 2nd/3rd degree AV block, cardiogenic shock, metabolic acidosis, severe peripheral arterial disease, phaechromocytoma.

Question 5

Side-effects?

Answer 5

GI disturbances, bradycardia, heart failure, hypotension, conduction disorders, peripheral vasoconstriction (including exacerbation of intermittent claudication and Raynaud’s phenomenon), bronchospasm, dyspnoea, headache, fatigue, sleep disturbances, paraesthesia, dizziness, vertigo, psychoses, sexual dysfunction, purpura, thrombocytopenia, visual disturbances, exacerbation of psoriasis, alopecia, rarely rashes and dry eyes.

Question 6

Possible interactions?

Answer 6

• Calcium channel blockers - Combined use of beta-blockers and calcium channel blockers with negative inotropic effects can lead to an exaggeration of these effects particularly in patients with impaired ventricular function and/or sinoatrial or atrioventricular conduction abnormalities. This may result in severe hypotension, bradycardia and cardiac failure.
• Dihydropyridines - Concomitant therapy may increase the risk of hypotension, and cardiac failure may occur in patients with latent cardiac insufficiency.
• Digitalis glycosides, in association with beta-blockers, may increase atrioventricular conduction time.
• Class I antiarrhythmic agents - May have potentiating effect on atrial-conduction time and induce a negative inotropic effect.
• Sympathomimetic agents - e.g. adrenaline, may counteract the effect of beta-blockers.
• Concomitant use with insulin and oral antidiabetic drugs may lead to the intensification of the blood sugar lowering effects of these drugs. Symptoms of hypoglycaemia, particularly tachycardia, may be masked.
• Prostaglandin synthetase-inhibiting drugs - e.g. ibuprofen and indomethacin, may decrease the hypotensive effects of beta-blockers.
• Amiodarone: Combination with atenolol may result in additive depressant effects on conduction and negative inotropic effects, especially in patients with underlying sinus node dysfunction or atrioventricular node dysfunction.
• Ampicillin: May reduce the bioavailability of atenolol. Therefore the physician should watch for evidence of altered atenolol response especially when large doses of ampicillin are administered concomitantly
• Peripheral muscle relaxants (e.g. Suxamethonium halogenide, Tubocurarine): concomitant use of atenolol could increase and extent the relaxative effect of muscle relaxants.

Question 7

Elimination?

Answer 7

The elimination half-life of oral atenolol is approximately 6 to 7 hours, and there is no alteration of the kinetic profile of the drug by chronic administration. When renal function is impaired, elimination of atenolol is closely related to the glomerular filtration rate; significant accumulation occurs when the creatinine clearance falls below 35 mL/min/1.73m2