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

Abstract An infusion of corticotropin-releasing factor (CRF, 0.1–5.0 μ g/10 μ l/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 μ g/10 μ l)-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 μ g/10 μ l). The increase in the splenic sympathetic nerve activity induced by CRF was not blocked by pretreatment with a cyclooxygenase inhibitor, sodium salicylate (100 μ g/10 μ l). In contrast, the splenic sympathetic nerve activity also increased after an i.c.v. injection of prostaglandin E 2 (PGE 2 , 1 ng/10 μ l) 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.