Blockade of the actions of the sympathetic neurotransmitter norepinephrine and the neurohormone epinephrine at α- and β-adrenoceptors has represented an important mechanism in drug therapy for decades, with a vast array of agonists and antagonists developed as therapeutic agents (e.g., β-adrenoceptor antagonists for hypertension, angina, and secondary prevention of acute myocardial infarction; β2-adrenoceptor agonists as bronchodilators in asthma and other bronchospastic conditions; α2-adrenoceptor agonists as well as α1-adrenoceptor antagonists for hypertension). Subtypes of each major class of adrenoceptors have been known for many years (β-adrenoceptors first subdivided in 1967, α-adrenoceptors initially subdivided in 1973), and recent identification of additional subtypes (e.g., β3-adrenoceptor for diabetes and obesity, further subdivision of α1-adrenoceptors for prostatic urethral obstruction) has stimulated increased interest in the design of subtype-selective agents. Molecular biological techniques facilitated the discovery of some subtypes (e.g., additional α1- and α2-adrenoceptor subtypes), while classical pharmacological techniques identified others (e.g., β3-adrenoceptor) and selective agents were synthesized and evaluated in humans before receptor sequencing. Subtype-selective agents often result in more efficacious drugs (e.g., α1-adrenoceptor selective prazosin for hypertension), and the recent proliferation of subtypes is likely to improve therapy. This review covers the molecular biology and classification of α- and β-adrenoceptors, including cloning and characterization of α1, α2, and β subtypes, their pharmacologic profiles, tissue distribution, and nomenclature.