The physiological relevance of the recently described prolactin-releasing p
eptides (PrRPs) has yet to be established. Hen, we demonstrate the low pote
ncy of the PrRPs (minimum effective dose: 100 nM), compared to that observe
d for thyrotropin-releasing hormone (TRH, minimum effective dose: 1.0 nM),
to stimulate prolactin (PRL) release from cultured pituitary cells harveste
d from lactating female rats. Anatomic studies question the role of these p
eptides in neuroendocrine control of lactotroph function. Instead, peptide
and peptide receptor mapping studies suggest potential actions in hypothala
mus and brainstem unrelated to the control of anterior pituitary hormone se
cretion. Intracerebroventricular (i.c.v.) administration of both PrRP-20 an
d PrRP-31 (0.4 and 4.0 nmol) resulted in significantly increased mean arter
ial blood pressure in conscious, unrestrained rats [peak elevations vs, bas
eline: PrRP-20, 10% and 16%, low and high dose peptide; PrRP-31, 7% and 10%
; compared to the response to 0.1 nmol angiotensin II (A II), 15-17%]. Simi
lar doses of peptide did not significantly alter water drinking in response
to overnight fluid deprivation, or thirst or salt appetite in response to
an isotonic hypovolemic challenge. Thus, the effect on blood pressure appea
red relatively specific. We suggest that these peptides, identified origina
lly as ligands for a receptor found in abundance in pituitary gland, play a
broader role in brain function and that the ability of them to stimulate P
RL release may not represent their primary biologic function. (C) 2000 Else
vier Science B.V. All rights reserved.