Sympathomimetics reproduce one or more effects of sympathetic activation through direct adrenergic-receptor agonism, promotion of catecholamine release, inhibition of reuptake or mixed mechanisms.

Direct drugs activate alpha or beta G-protein-coupled receptors. Indirect drugs increase synaptic catecholamines by release or reuptake inhibition; physiological response depends on receptor selectivity, dose, route and baseline autonomic tone.

Important examples are epinephrine, norepinephrine, dopamine, dobutamine, phenylephrine, ephedrine, pseudoephedrine, salbutamol, terbutaline, clonidine and amphetamine.

Uses include anaphylaxis, shock, cardiac support, bronchospasm, hypotension, nasal congestion, attention-deficit disorders and selected ophthalmic or obstetric indications. Choice must match receptor profile and clinical goal.

Excess sympathetic stimulation causes anxiety, tremor, insomnia, tachycardia, arrhythmia, hypertension and ischaemia. Alpha-2 agonists instead commonly cause sedation, bradycardia and dry mouth; beta-2 agonists can cause hypokalaemia.

Caution is required in coronary disease, arrhythmia, severe hypertension, hyperthyroidism and with drugs that amplify catecholamine effects. Extravasated vasopressors can cause tissue ischaemia.