Estradiol Inhibits Plasma Somatostatin 14 (SRIF-14) Levels and Inhibits the Response of Somatotrophic Cells to SRIF-14 Challengein Vitroin Rainbow Trout,Oncorhynchus mykiss

In the present study, the effects of 17 beta-estradiol (E2) treatment on plasma growth hormone (GH) and somatostatin 14 (SRIF-14) concentrations were investigated, as well as the effect of in vivo E2 treatment on the in vitro GH response to SRIF-14 challenge in sexually immature rainbow trout (Oncorhynchus mykiss). Two weeks after receiving a steroid hormone implant, plasma E2 and GH levels were significantly (P < 0.05) elevated, and plasma SRIF levels were significantly (P < 0.05) lowered relative to the control. Pituitary glands were taken from E2-primed and control fish and challenged with a single pulse of SRIF-14 (10(-8) M) in a perifusion unit to evaluate the effect of E2 on the response of somatotrophs to the effect of SRIF-14. Whereas SRIF-14 challenge significantly (P < 0.01) inhibited GH release from pituitary fragments taken from control fish, there was no such response in E2-primed fish. Furthermore, GH release following SRIF-14 administration (at the point of maximal inhibition) was significantly depressed in control fish with respect to the E2 treatment group. These data suggest that E2 treatment may increase plasma GH concentrations by altered somatotroph responsiveness to SRIF-14 inhibition. Furthermore, E2 may increase plasma GH by suppressing plasma SRIF-14 levels, although the role of circulating SRIF-14 on the regulation of GH release has not been fully determined in teleosts.