Widely used in treatment of ischaemic heart disease and hypertension across the world. All have different affinities for beta-1 and beta-2.
|Drug||Beta-1 cardioselectivity||Intrinsic sympathomimetic activity|
All useful effects of beta blockers come from their beta-1 blockade, antagonism of beta-2 receptors gives unwanted side effects. (Review: Actions of adrenoceptors).
In theory beta blockers with intrinsic sympathomimetic activity (partial agonists) are less likely to cause severe bradycardia.
Negative inotropic and chronotropic
Sinoatrial node automacity decreased
Atrioventricular node conduction prolonged
Bradycardia increases coronary artery diastolic filling time
Class II antiarrhythmic agents
Inhibition of beta-1 receptors at juxtaglomerular apparatus reduces renin release and therefore reduces angiotensin II and aldosterone.
Inhibition of peripheral beta-2 receptors may cause an element of vasoconstriction: Responsible for side effects of cold hands and impotence.
All beta blockers given at a high enough dose will cause bronchospasm through beta-2 antagonism
Non-selective beta blockers can obtund normal blood glucose response to exercise
May mask symptoms of hypoglycaemia
Lipid soluble beta blockers (metoprolol and propranolol) more likely to cause side effects e.g. nightmares, fatigue.
Decreased production of aqueous humour, decreases intra-ocular pressure.