The aim of this thesis was to investigate hypothalamic-pituitary
control by measuring the release of neuropeptides into pituitary stalk
blood. The neuropeptides measured were luteinizing hormone-releasing
hormone (LHRH) and the 'gut peptides' cholecystokinin (CCK), gastrin
and vasoactive intestinal polypeptide (VIP). Studies in castrated rats showed that, (1) despite marked increases
in pituitary gonadotro_phin secretion and the number of LHRH receptors
in the anterior pituitary gland, the amount of LHRH in stalk blood was
similar to that in control rats; (2) the release of LHRH into stalk blood
induced by electrical stimulation of the median eminence (ME) was
significantly lower than in control rats; (3) administration of oestradiol,
5a-dihydrotestosterone or testosterone (T), suppressed the post-castration rise in plasma luteinizing hormone (LH) but had no effect on LHRH
released into stalk blood or the increased number of LHRH receptors
in the anterior pituitary gland. Experiments using intact and castrated rats made hyperprolactinaemic
by implanting two anterior pituitary glands under the kidney
capsule showed that, (1) the suppression of gonadotrophin release in
intact and castrated hyperprolactinaemic rats was not accompanied by
a decrease in LHRH release into stalk blood; (2) electrical stimulation
of the ME was as effective in hyperprolactinaemic rats as in control rats
in increasing LHRH release into stalk blood; (3) implantation of T
capsules into castrated hyperprolactinaemic rats suppressed gonadotrophin but not LHRH secretion. Catechol oestrogens stimulated the release of LH in pre-pubertal
male and female rats but suppressed LH release induced by pregnant
mare serum gonadotrophin. CCK and VIP, but not gastrin, were released in significantly
higher concentrations into stalk blood than into peripheral blood of
adult male rats. Electrical stimulation of several areas of the brain
known to contain CCK, gastrin or VIP did not alter the release of these
peptides. Removal of the major peripheral source of CCK and gastrin
(the gastric antrum) or VIP (the entire gut), significantly lowered
CCK and gastrin concentrations but did not reduce VIP release into
stalk blood. VIP release into stalk blood at various times of the oestrous
cycle under Althesin, Ketalar, Sagatal or urethane anaesthesia showed
no clear-cut changes. Therefore, it is unlikely that CCK and gastrin
are physiological hypothalamic-pituitary regulatory factors. The
physiological significance of the higher amounts of VIP in stalk blood
compared with peripheral blood remains to be determined
