Acute intravenous administration of either clonidine (Clon) (50 micrograms kg-1) or desipramine (DMI) (5 mg kg-1) elicited a pulse of growth hormone (GH) and corticosterone secretion in conscious, unrestrained rats. 2. The responses to DMI were similar to those with Clon, except that the GH pulse following DMI was delayed and was not dose-dependent. 3. The GH response to DMI was inhibited by prior administration of idazoxan (1 mg kg-1) or yohimbine (0.5 mg kg-1), but not by atropine (10 micrograms kg-1), sulpiride (5 mg kg-1) or prazosin (1 mg kg-1). 4. The corticosterone secretion following DMI was not altered by prior atropine, sulpiride or prazosin, but was augmented by idazoxan (1 mg kg-1). 5. GH secretion was not influenced by atropine, sulpiride, prazosin or idazoxan given alone. Idazoxan or yohimbine given alone elicited significant secretion of corticosterone. 6. It is concluded that i.v. DMI caused an activation through indirect mechanisms of alpha 2-adrenoceptors specifically involved in hypothalamic-pituitary regulation of GH release and also a distinct, independent and transient generalized activation of the pituitary-adrenal axis.
