A. Kjaer et al., INVOLVEMENT OF VASOPRESSIN IN HISTAMINE-INDUCED AND STRESS-INDUCED PROLACTIN-RELEASE - PERMISSIVE, MEDIATING OR POTENTIATING ROLE, Neuroendocrinology, 57(2), 1993, pp. 314-321
Arginine vasopressin (AVP) appears to be involved in the histamine (HA
)- and stress-induced prolactin (PRL) release. The present investigati
on was performed in male rats to clarify whether the role of AVP in HA
- and restraint stress-induced secretion of PRL is mediating (i.e., th
e effect of HA or stress is transmitted via AVP) or permissive (i.e.,
the presence of AVP is required to obtain a stimulatory effect of HA o
r stress on PRL secretion). Furthermore, we studied whether AVP posses
sed a potentiating effect on the HA- or stress-induced PRL release. PR
L secretion was stimulated 14- to 17-fold by intracerebroventricular i
nfusion of HA (270 nmol) or by 5 min of restraint stress. These effect
s were inhibited about 80% by immunoneutralization of endogenous AVP w
ith a specific AVP antiserum (abAVP). When specific AVP V1- or V2-rece
ptor agonists, which were not bound by the AVP antiserum, were adminis
tered intravenously together with the AVP antiserum, the PRL response
to HA or restraint stress was partly (> 50%) reestablished. This effec
t was observed at low (1.2 or 0.1 nmol) as well as high (3.8 or 0.4 nm
ol) doses of agonists and when these were administered alone or in com
bination. In non-immunoneutralized animals, separate administration of
agonists at low or high doses as well as combined administration of a
gonists at low doses had no or only a minor effect on PRL secretion, w
hile combined administration of V1- and V2-agonist in high doses stimu
lated PRL secretion 6-fold. Taken together, these observations indicat
e that AVP has a permissive role. Since the response to HA or restrain
t stress was only partly reestablished by AVP agonists, it appears tha
t AVP plays a mediating role as well. When AVP was administered in a d
ose (240 pmol) which had no PRL-releasing effect in itself, the PRL-st
imulating effect of a submaximal HA dose or restraint stress was not a
ltered. This excludes a potentiating effect of AVP. We suggest that AV
P (probably of hypothalamic origin) has a permissive and probably also
a mediating effect on the PRL response to HA or restraint stress.