Interaction Between Dexmedetomidine and α-Adrenergic Receptors: Emphasis on Vascular Actions

p Dexmedetomidine (DEX) is a new methylol derivative with high affinity to 2-adrenergic receptors. It causes analgesia and sympatholysis, and has sedative, anxiolytic, and hypnotic effects. The use of DEX and its affinity to 2-adrenergic eceptors in the body should not only be limited to sedation and nesthesia, because 2-adrenergic receptors are scattered hroughout the body. In 1948, Ahlquist et al1 first reported and subtypes of adrenergic receptors that were activated by noradrenalin, the mediator of sympathetic nervous system stimulation in mammals. In light of this preliminary report, numerous studies were performed on this topic and, in 1973, 1 and 2 subtypes of -adrenergic receptors were determined.2 In subsequent investigations, gene studies were developed, and 3 subtypes, called aA, 1B, and 1c, or 1-adrenergic receptors2 and 4 subtypes, called 2A, 2B, 2C, and 2D, for 2-adrenergic receptors were isolated.3,4 Studies perormed on isolated organ samples from several experimental anmals showed that both subtypes of -adrenergic receptors are present in postsynaptic membranes in many animal species, including rabbits and guinea pigs; 1-adrenergic receptors are domnant.5 In contrast, 2-adrenergic receptors were reported to be enser only in a number of tissues, such as human saphenous vein6 and femoral vein tissue.7 Experimental findings show that localization of -adrenergic receptor subtypes can differ among species nd vessel segments, so the responses that occur after activation of hese receptors vary.