Beta-blockers in hypertension and beta-1 blockade

Sympathetic drive (the 'fight or flight' nerve signals) speeds up the heart through beta-1 receptors. Atenolol, bisoprolol and metoprolol are beta-blockers that occupy these receptors, so the heart beats more slowly and each beat is weaker, which is lower contractility (the force of each beat).

With a slower, weaker pump, less blood moves each minute, so cardiac output falls and pressure falls with it. The kidney adds to the effect: beta-1 receptors there help trigger the release of renin, an enzyme that starts a hormone chain raising blood pressure, so blocking them lowers renin. The exact mechanisms behind the fall in blood pressure are still not fully understood.

Slowing the heart also lowers the oxygen it needs. That makes a beta-blocker a good fit for angina (chest pain caused when the heart muscle gets too little oxygen). In NICE guidance, beta-blockers are no longer first-line (the drug tried first) for uncomplicated hypertension, but they remain useful when ischaemic heart disease (heart disease caused by narrowed coronary arteries) or heart failure coexists.

Side effects follow from blocking beta receptors, and bronchospasm in particular can follow from blocking beta-2 receptors in the airways, which normally keep them relaxed. Bradycardia (a slow pulse), fatigue and cold hands and feet are side effects, as is bronchospasm (tightening of the airway muscle, causing wheeze and breathlessness). Selective drugs such as bisoprolol, which mainly block beta-1 receptors, are safer than non-selective ones but not entirely safe, so asthma is a relative contraindication (a reason for caution rather than an absolute ban), although in severe asthma the contraindication is absolute.

Alpha-blockers such as doxazosin work differently. They block alpha-1 receptors on blood vessels, causing vasodilation, and the major side effect is postural hypotension (blood pressure falling on standing up, causing dizziness), particularly with the first dose.