ADRENERGIC REGULATION OF THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS UNDER BASAL AND SOCIAL STRESS CONDITIONS

The significance of adrenergic neurons and anterior pituitary and hypo thalamic adrenergic receptors in stimulation of the hypothalamic-pitui tary-adrenal (HPA) axis by corticotropin releasing hormone (CRH) and v asopressin (AVP) was investigated under basal conditions and after thr ee-days crowding stress in conscious rats. In nonstressed rats the cor ticosterone response to phenylephrine, an alpha(1)-adrenergic receptor agonist, was totally abolished or considerably reduced by prazosin, a n alpha(1)-receptor antagonist, when both those drugs were given ip or icv, respectively. The corticosterone response to ip isoproterenol, a beta-adrenergic agonist, was abolished by icy or ip pretreatment with propranolol, a beta-adrenergic receptor antagonist. These results ind icate involvement of functional alpha(1)-adrenoceptors in the hypothal amus and anterior pituitary corticotrops and pituitary beta-adrenocept ors in stimulation of the HPA axis. AVP given ip was almost as potent as CRH in stimulating corticosterone secretion. The stimulatory effect of AVP given ip or icv on corticosterone secretion was significantly diminished by propranolol, but not prazosin or yohimbine, indicating a n involvement of beta-adrenergic receptors. The specific noradrenergic neurotoxin DSP-4, given ip 11 days before the experiment, considerabl y diminished the hypothalamic noradrenaline (NA) level but did not inf luence the resting and icy CRH- or AVP-stimulated corticosterone secre tion. In nonstressed rats CRH further enhanced significantly the DSP-4 -elicited fall in hypothalamic NA, whereas AVP almost totally prevente d that decrease. In stressed rats CRH considerably antagonized the DSP -4-induced decrease in the hypothalamic NA level while AVP did not aff ect that decrease. The CRH- and AVP-elicited changes in hypothalamic N A were not correlated with changes in corticosterone secretion. Tree-d ay crowding stres did not affect the CRH-induced corticosterone secret ion, whereas it considerably reduced the AVP-evoked corticosterone res ponse. These results indicate that pituitary and hypothalamic adrenerg ic receptors are significantly involved in the AVP- and CRH-induced HP A axis stimulation, but the hypothalamic NA level, though modified by these peptides, does not significantly influence the HPA response.