Sequential relationship between actions of CRF and PGE2 in the brain on splenic sympathetic nerve activity in rats

An infusion of corticotropin-releasing factor (CRF, 0.1-5.0 micrograms/10 microliters/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 + alpha-chloralose anesthetized rats. No changes in the arterial blood pressure and body temperature were observed. The CRF (1.0 micrograms/10 microliters)-induced enhancement of the splenic sympathetic nerve activity was completely blocked by an i.c.v. pretreatment with a CRF antagonist, alpha-helical CRF9-41 (alpha-hCRF, 10 micrograms/10 microliters). The increase in the splenic sympathetic nerve activity induced by CRF was not blocked by pretreatment with a cyclooxygenase inhibitor, sodium salicylate (100 micrograms/10 microliters). In contrast, the splenic sympathetic nerve activity also increased after an i.c.v. injection of prostaglandin E2 (PGE2, 1 ng/10 microliters) and the increase was completely blocked by i.c.v. pretreatment with alpha-hCRF. These findings suggested a sequential relationship between actions of CRF and PGE2, with an activation of PGE2 system followed by that of CRF system in the brain resulting in an increase in the splenic sympathetic nerve activity.