The role of central arginine vasopressin in corticotropin releasing hormone-induced fever in rats.

The purpose of the present study was to investigate the role of central arginine vasopressin (AVP) in corticotropin releasing hormone (CRH) induced fever in the rat. Guide cannulae were inserted into the third ventricle and placed over the ventral septal area (VSA). The content of arginine vasopressin in the VSA of the brain was determined by radioimmunoassay. Colon temperature was monitored in lightly restrained rats by insertion of a catheter mounted thermistor probe 5 cm in the rectum. The results demonstrated that intracerebroventricular (icv) injection of CRH increased AVP level in the VSA and the colonic temperature of the rats. Microinjection of AVP V(1) antagonist into the VSA 10 min before CRH administration significantly enhanced CRH-induced febrile response, while AVP V(1) antagonist itself did not have a significant effect on the colonic temperature. Furthermore, injection of AVP into the VSA 5 min before CRH administration (icv) suppressed the fever evoked by CRH. These findings suggest that CRH is an important factor that stimulates the release of AVP in the VSA during fever, and endogenous AVP in the VSA has an antipyretic action on the CRH-induced fever.

[Antipyretic action of dexamethasone on egtazic acid-induced fever in rabbits].

The purpose of the present study was to investigate whether the antipyretic effect of dexamethasone (DEX) delivered by intravenous injection (i.v.) on intracerebroventricularly (icv) administered egtazic acid-induced febrile response is relevant to the changes in cytosolic free calcium concentration of the hypothalamus. The colon temperatures were measured by a thermistor and the cytosolic free calcium concentration ([Ca2+]i) in dissociated brain cells was measured by Fura 2-AM. The results demonstrated that the pyretic action of egtazic acid (0.6 mumol, icv) was markedly inhibited by DEX (5 mg/kg, i.v.), but DEX (60-120 mumol/L) did't affect [Ca2+]i in dissociated hypothalamus cells. Actinomycin D, which interferes with gene transcription (3 nmol, icv), completely abolished the antipyretic action of DEX on egtazic acid-induced fever. These findings suggest that the antipyretic action of DEX on egtazic acid-induced fever is related to the activation of certain gene expression in the brain, but not to the changes of transmembrane calcium ion current in hypothalamus neurons.