AUTONOMIC PHARMACOLOGY OF ALPHA(2)-ADRENOCEPTORS

alpha(2)-Adrenoceptors are widely distributed in the body: they occur on neurones, and on smooth muscle, gland, fat, epithelial and blood ce lls. Neuronal alpha(2)-adrenoceptors are located either on the noradre nergic neurones themselves ('autoreceptors') or on neurones using neur otransmitters other than noradrenaline ('heteroreceptors'). Neuronal a lpha(2)-adrenoceptors play an important role in autonomic regulation. The stimulation of central alpha(2)-adrenoceptors by appropriate agoni sts (e.g. clonidine) leads to an overall decrease in sympathetic activ ity reflected both in a reduction in impulse traffic in peripheral sym pathetic fibres and in the plasma concentration of noradrenaline. The activation of central alpha(2)-adrenoceptors leads to a reduction in b lood pressure and heart rate, and may be associated with an increase i n vagal activity. Central alpha(2)-adrenoceptor activation results in an impairment of thermoregulation leading either to a drop or an incre ase in body temperature depending on the ambient temperature. Central alpha(2)-adrenoceptors contribute to the regulation of pupil size and the kinetics of the pupillary light reflex. The activation of alpha(2) -adrenoceptors on central noradrenergic neurones leads to miosis consi stent with the sympatholytic effect of alpha(2)-adrenoceptor agonists, whereas activation of postsynaptic alpha(2)-adrenoceptors on neurones in the Edinger-Westphal nucleus results in mydriasis. alpha(2)-Adreno ceptor agonists reduce salivary secretion probably by a direct action at postsynaptic alpha(2)-adrenoceptors on parasympathetic salivary neu rones in the brainstem. Two sympathetically mediated activities, sweat gland secretion and physiological finger tremor, are unaffected by az -adrenoceptor agonists,indicating that alpha(2)-adrenoceptors are not involved in the regulation of these functions.