Abstract
An infusion of corticotropin-releasing factor (CRF, 0.1–5.0 μg/10 μl/rat) into the third cerebral ventricle (i.c.v.) for 10 min increased the splenic sympathetic nerve activity in a dose-dependent manner in urethane+ α-chloralose anesthetized rats. No changes in the arterial blood pressure and body temperature were observed. The CRF (1.0 μg/10 μl)-induced enhancement of the splenic sympathetic nerve activity was completely blocked by an i.c.v. pretreatment with a CRF antagonist, α-helical CRF 9–41 ( α-hCRF, 10 μg/10 μl). The increase in the splenic sympathetic nerve activity induced by CRF was not blocked by pretreatment with a cyclooxygenase inhibitor, sodium salicylate (100 μg/10 μl). In contrast, the splenic sympathetic nerve activity also increased after an i.c.v. injection of prostaglandin E 2 (PGE 2, 1 ng/10 μl) and the increase was completely blocked by i.c.v. pretreatment with α-hCRF. These findings suggested a sequential relationship between actions of CRF and PGE 2, with an activation of PGE 2 system followed by that of CRF system in the brain resulting in an increase in the splenic sympathetic nerve activity.
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