beta-blocker

A beta-blocker takes the foot off the heart's accelerator. The stress chemicals adrenaline and noradrenaline normally hit beta-adrenoceptors to make the heart beat faster and harder, the way pressing a gas pedal revs an engine. A beta-blocker sits on those receptors and shields them, so the heart settles into a slower, gentler rhythm and uses less oxygen.

These drugs are competitive antagonists at beta-adrenoceptors. Blocking beta-1 receptors in the heart reduces heart rate, contractility and conduction velocity, lowering cardiac output and oxygen demand; many also reduce renin release from the kidney. Members end in -olol, including atenolol, metoprolol, bisoprolol, propranolol and carvedilol. They are used in hypertension, angina, certain arrhythmias, after a heart attack, and in stable chronic heart failure, where carefully introduced beta-blockade improves survival.

Selectivity matters: cardioselective agents such as bisoprolol act mainly on beta-1, whereas non-selective agents such as propranolol also block beta-2 receptors in the airways and can provoke bronchospasm, so they are used cautiously in asthma. Other cautions include masking the warning signs of hypoglycaemia in diabetics, fatigue and cold extremities, and the need to taper rather than stop abruptly, since sudden withdrawal can trigger rebound tachycardia or angina.