Abstract: | Injection of SRIF antiserum (oA-SRIF) increases serum GH and TSH levels in urethane-anesthetized rats. These responses require an intact hypothalamus with endogenous GH-releasing factor (GHRF) or TRH, respectively. We examined whether pretreatment of rats with an antiserum against rat GHRF (oA-rGHRF) would abolish the GH response to oA-SRIF, since anti-TRH serum has been shown to abolish TSH response to oA-SRIF. Prior injection of oA-rGHRF reduced oA-SRIF-induced GH response in a dose-related manner in a dose up to 1 ml antiserum, but failed to produce any further suppression at higher doses. The maximum suppression of the GH response was approximately 50%. oA-rGHRF also suppresses basal GH levels significantly. On the other hand, oA-rGHRF completely abolished the GH-releasing activity of 1 microgram synthetic rGHRF when incubated for 30 min at room temperature before injection. The results suggest two conclusions: 1) 43-residue rGHRF is a physiological regulator of both basal and stimulated GH release; 2) failure of oA-rGHRF to completely abolish the GH response to oA-SRIF suggests the presence of other physiological GHRFs in the rat. |