Gonadotropin-releasing hormone-associated peptide exerts a prolactin-inhibiting and weak gonadotropin-releasing activity in vivo.

The in vivo effects of GnRH-associated peptide (GAP) on PRL, LH, and FSH release have been examined by injecting this peptide iv into the following types of conscious rats: 1) ovariectomized steroid-blocked females, 2) ether-stressed males, and 3) lactating females. GAP (2.4 X 10(-10) and 2.4 X 10(-9) mol) suppressed plasma PRL release but did not affect the levels of plasma LH and FSH in ovariectomized steroid-blocked rats. Furthermore, with 1-min etherization, GAP (1.6 X 10(-10) and 8.0 X 10(-10) mol) reduced the stress-induced rise of plasma PRL, but had no effect on the stress-induced decline of plasma gonadotropin levels in male rats. A single iv injection of GAP (8.0 X 10(-10) mol) into lactating rats before the onset of nursing did not block the elevation of plasma PRL induced by suckling. However, a second injection of GAP (1.6 X 10(-10) mol) at 30 min after the onset of suckling partially lowered plasma PRL levels 15 min later. By contrast, plasma FSH levels were significantly elevated by the second injection of GAP, and plasma LH also rose after iv administration of GAP in the nursing rats. These results indicate that the activity of GAP to stimulate FSH and LH release is limited, since GAP stimulated the release of FSH and LH only when plasma gonadotropin levels were extremely low. However, the in vivo evidence that GAP inhibited PRL release in a variety of conditions reinforces the possibility that GAP could be the peptidic PRL-inhibiting factor.