Substance P and various opiate receptor activators were injected into the lateral ventricle of urethane anesthetized male rats which were pretreated with either normal sheep serum (NSS), sheep antiserum to somatostatin (anti SS), or rabbit antiserum to substance P (anti SP). The injection of substance P (10-9 mol) suppressed serum GH levels, but not PRL levels, in both NSS and anti SP pretreated rats, whereas the suppressive effect was not observed in animals pretreated with anti SS. In both NSS and anti SS pretreated rats, β endorphin (10-10 and 10-9 mol) and D [Ala2]enkephalin amide (10-9 mol) stimulated both GH and PRL release, whereas α and γ endorphins, [Met5]enkephalin, and morphine sulfate (10-9 mol) induced only a meager GH response, but a significant PRL response. Simultaneous injection of β endorphin (10-10 or 10-9 mol) and substance P (10-9 mol) caused greater GH and PRL responses than did β endorphin alone in rats pretreated with either NSS, anti SS, or anti SP. Both GH and PRL responses to morphine sulfate (10-9 mol) plus substance P (10-9 mol) were larger than those to morphine sulfate alone. Naloxone (10-9 mol) not only inhibited both GH and PRL release induced by β endorphin (10-10 mol), but also blocked the synergistic effect of substance P on both GH and PRL responses to β endorphin. These results suggest the following: first, the intraventricular administration of substance P may stimulate hypothalamic somatostatin release into the portal vessels, thereby decreasing GH secretion; second, the opiate receptor activator stimulates GH and PRL release by a mechanism which does not involve endogenous somatostatin; third, substance P may potentiate the action of opiate receptor stimulators on GH and PRL release at the central nervous system.
ASJC Scopus subject areas