ABSTRACT
Psychopharmacology Unit, University of Bristol, Bristol, U.K. and Department of Pharmacology, Medical Sciences Building, University of Alberta, Edmonton, Canada
INTRODUCTION
The adrenoceptors belong to the large family of seven transmembrane (TM) G-protein-linked receptors. The very fact that adrenoceptors are coupled to G-proteins is the primary mechanism for allosteric interaction that results in intracellular changes to elicit a biological response. They are cell membrane receptors and mediate the effects of the endogenous catecholamines, adrenaline, and noradrenaline. The adrenoceptor family has been subdivided into three pharmacologically and functionally distinct subgroups. The major subgroups of adrenoceptor are now classified as the a1-adrenoceptors, a2adrenoceptors and b-adrenoceptors (1-3). The subdivision of the a-adrenoceptors was initially based on anatomical location and the discovery of prejunctional autoreceptors, which regulate the release of noradrenaline. Langer (4) proposed that a-adrenoceptors in the sympathetic nervous system could be subdivided into a1-adrenoceptors, located postsynaptically,
and a2-adrenoceptors, which were located presynaptically and regulated the release of noradrenaline through a negative feedback system. However, the pharmacological characterization of the a-adrenoceptor subtypes resulted in the identificationof the ‘‘presynaptic’’a2-adrenoceptor in apostsynaptic location and, thus, a1-and a2-adrenoceptors were characterized pharmacologically rather than anatomically (5).
