The control of the release of some hypophysial portal vessel peptides
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.