SELECTIVE-INHIBITION OF MAGNOCELLULAR VASOPRESSIN NEURONS BY HYPOOSMOLALITY - EFFECT ON HISTAMINE-INDUCED AND STRESS-INDUCED SECRETION OF ADRENOCORTICOTROPIN AND PROLACTIN
A. Kjaer et al., SELECTIVE-INHIBITION OF MAGNOCELLULAR VASOPRESSIN NEURONS BY HYPOOSMOLALITY - EFFECT ON HISTAMINE-INDUCED AND STRESS-INDUCED SECRETION OF ADRENOCORTICOTROPIN AND PROLACTIN, Neuroendocrinology, 67(5), 1998, pp. 330-335
We investigated the effect of selective inhibition of magnocellular ar
ginine vasopressin (AVP) and oxytocin neurons on histamine (HA)- and r
estraint-stress-induced adrenocorticotropin (ACTH) and prolactin (PRL)
secretion in conscious male rats. The inhibition of magnocellular neu
rons was obtained by inducing chronic hypoosmolality via continuous ex
posure of the rats to the AVP V-2 receptor agonist 1-deamino(8-D-argin
ine)vasopressin (DDAVP) which was released from osmotic pumps implante
d subcutaneously. In DDAVP-treated rats, plasma osmolality and sodium
concentration were 273 mosm/l and 130 mmol/l, respectively. In control
rats, the corresponding values were 291 mosm/l and 139 mmol/l. HA (27
0 nmol) administered intracerebroventricularly or 5 min of restraint s
tress stimulated ACTH and PRL secretion 4- to 11-fold in normoosmolar
rats. In hypoosmolar rats, the HA-induced ACTH response was inhibited
more than 40% whereas the restraint-stress-induced ACTH response was u
naffected. Conversely, the PRL response to HA in hypoosmolar rats was
unaffected whereas the PRL response to restraint stress was inhibited
by 40%. In summary, chronic hypoosmolality inhibits HA-induced ACTH an
d restraint-stress-induced PRL secretion indicating involvement of mag
nocellular AVP in these responses.