Abstract
Alpha 2-adrenergic receptors mediate adrenergic stimulation of growth hormone (GH) secretion in the rat. The GH response to the alpha 2-adrenergic agonist clonidine has thus been used as an index of alpha 2-adrenergic receptor responsiveness. Pharmacologic manipulations known to upregulate alpha 2-adrenergic receptor sensitivity would then be expected to result in an enhancement of the GH response to clonidine. To test this hypothesis, rats were injected in the lateral ventricle with either 6-hydroxydopamine or sterile saline. One month following the lesion, urethane-anesthetized rats from each group were administered clonidine or saline. Venous samples for plasma GH were drawn prior to or following the clonidine or saline administration. Rats administered clonidine had greater GH responses than those administered saline within either the lesioned or nonlesioned groups. The GH response to clonidine was significantly greater in the lesioned group than in the nonlesioned group. As 6-hydroxydopamine pretreatment upregulates alpha 2-adrenergic receptors, these results support the validity of the use of the GH response to clinidine as an index of alpha 2-adrenergic receptor responsiveness.
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