Biomedical subjects

R A Prysor-Jones

Publications and source records attributed to R A Prysor-Jones.

25 records · Page 2Linked to original sources

PubMed1983

Hypothalamic dopamine and catechol oestrogens in rats with spontaneous pituitary tumours.

Dopamine concentration within the hypothalamus and its depletion after the administration of alpha-methyl-para-tyrosine were measured in young rats and compared with values obtained in aged animals with and without spontaneously occurring pituitary tumours. Old rats had significantly reduced hypothalamic dopamine concentrations and there was less depletion of dopamine compared with young animals but there were no differences between tumorous and non-tumorous animals. Hyperprolactinaemia induced in young animals caused a much greater depletion of hypothalamic dopamine than in old tumorous rats with comparable plasma prolactin concentrations. The catechol oestrogen 2-hydroxyoestradiol inhibited the release of prolactin from normal rat pituitary glands in vitro but measurement of catechol oestrogens in the hypothalamus showed no differences between young and old tumorous or non-tumorous rats. It is concluded that reduced dopamine concentration and an impaired response to hyperprolactinaemia in old rats may facilitate the growth of prolactin-secreting tumours arising in the pituitary gland.

Adenoma↗

PubMed1983

Effect of tamoxifen on growth and prolactin secretion of rat pituitary tumours.

The antioestrogenic drug tamoxifen was administered to rats bearing transplanted prolactin-secreting tumours derived from spontaneously occurring pituitary adenomas in Wistar-Furth rats. Some inhibition of tumour growth was observed but this was accompanied by an increase in plasma prolactin concentrations. Bromocriptine, however, consistently inhibited both growth and prolactin secretion of these tumours. The addition of tamoxifen to bromocriptine treatment produced no increased response to the dopamine agonist. Tamoxifen increased prolactin secretion by tumour cells in vitro but did not affect DNA synthesis. Normal rats responded to tamoxifen with a moderate increase in plasma prolactin concentrations and there was no change in pituitary DNA synthesis.

Animals↗

PubMed1982

The effect of chronic neuroleptic treatment on gonadotrophin release.

Although neuroleptic-induced hyperprolactinaemia is a common cause of amenorrhoea in women, the mechanism by which ovarian function is disturbed is unknown. Previous studies on both hyperprolactinaemic women and rats have indicated that an impairment of the pituitary response to LH-RH may be involved. We have investigated this possibility in female psychiatric patients undergoing chronic treatment with depot neuroleptics. The patients and a group of healthy controls were subjected to a standard LH-RH provocation test. Basal and post-stimulation serum levels of gonadotrophins, prolactin and oestradiol were determined. We have found that the LH responses of the patients fell into three groups: exaggerated, normal and impaired. Differences in the basal levels of gonadotrophins were also observed. The abnormal basal hormone levels and LH-RH responses appear to be related to neuroleptic dose and/or serum prolactin concentration, but no well-defined relationship was found. The results suggest that an action of the neuroleptics which is independent of high serum prolactin levels may be involved in the disruption of pituitary function. Thus the amenorrhoea caused by neuroleptic drug treatment may be etiologically different from that of other forms of hyperprolactinaemic amenorrhoea.

Adult↗

PubMed1981

Effect of bromocriptine, somatostatin, and oestradiol-17 beta on hormone secretion and ultrastructure of human pituitary tumours in vitro.

The effect of bromocriptine and somatostatin on hormone secretion and the ultrastructure of human pituitary adenomas was studied in vitro. Prolactin secretion was inhibited by bromocriptine in 3 out of 10 prolactin-secreting tumours and in explants from 2 normal pituitaries. GH secretion was reduced by bromocriptine in 4 out of 6 GH-secreting adenomas but was not affected by the drug in the incubations of normal pituitaries. Somatostatin inhibited GH secretion in 2 out of 5 pituitary adenomas and the effect was comparable with that of bromocriptine. Incubation of prolactin-secreting adenomas with oestradiol for as long as 24 days produced no change in hormone secretion. Examination of tumour explants by electron microscopy showed that somatostatin and bromocriptine produced accumulation of secretion granules but no changes in the secretory organelles. Long term bromocriptine treatment of "nude" athymic mice bearing xenografts of human pituitary adenomas suppressed hormone secretion and produced some increase in secretion granules but there were no morphological changes in the secretory organelles or other vital structures of the adenoma cells.

Adenoma↗

PubMed1981

Effect of bromocriptine on DNA synthesis, growth and hormone secretion of spontaneous pituitary tumours in the rat.

The 'spontaneous' development of pituitary tumours has been studied in the Wistar-Furth strain of rat. In females aged 64--135 weeks the incidence was as high as 69% whereas in males aged 72--116 weeks only 6% developed tumours. Hyperprolactinaemia was invariably associated with these spontaneous pituitary tumours but excessive secretion of growth hormone (GH) was found in one animal only. Bromocriptine inhibited secretion of prolactin and DNA synthesis of the tumours. In a mixed GH- and prolactin-secreting tumour transplanted to a peripheral site, bromocriptine reduced the size of the tumour as well as the secretion of both hormones. Oestradiol reversed the inhibitory action of bromocriptine on prolactin secretion and tumour growth but failed to influence the reduction in GH secretion caused by the drug.

Animals↗

PubMed1980

Effect of excessive secretion of growth hormone on tissues of the rat, with particular reference to the heart and skeletal muscle.

Rat pituitary tumours of the GH3 cell line, secreting growth hormone (GH), were induced to grow in Wistar-Furth rats and the effect of prolonged excessive secretion of GH on various organs was investigated. Total body weight of the tumour-bearing animals increased by over 100% compared with control animals and there was widespread visceromegaly affecting especially the liver, kidney, spleen and adrenals. The heart was also considerably enlarged. The effects of excessive GH on skeletal muscle were not uniform and, using a histochemical technique, it was found that the size type 1 muscle fibres was increased to the greatest extent whereas fibre type 2A was unaffected. Synthesis of DNA in the heart and skeletal muscle was also increased in tumour-bearing animals. Removal of the tumours was followed by a considerable regression in the size of most organs, although hypertrophy of the heart was affected least by a return to normal plasma levels of GH. It was concluded that animals bearing GH3 cell tumours provide a useful experimental model for the study of the tissue changes in acromegaly.

Acromegaly↗

PubMed1980

Effect of bromocriptine, ergotamine and other ergot alkaloids on the hormone secretion and growth of a rat pituitary tumour.

The effect of bromocriptine on hormone secretion and the growth of the prolactin- and growth hormone (GH)-secreting rat pituitary tumour of the GH3 cell line has been compared with that of ergotamine and other ergot alkaloids. Bromocriptine in doses ranging from 1 to 20 mg/kg had no effect on tumour growth or on the excessive secretion of GH by the tumour; prolactin concentrations were reduced only by the highest dosage of the drug. Similarly the tumour was resistant to the administration of ergocryptine, ergocornine and the synthetic ergolines, lergotrile and CH 29-717. In contrast, ergotamine reduced secretion of both GH and prolactin and considerably inhibited the growth of the tumour. Experiments in vitro showed that ergotamine inhibited DNA synthesis of the tumour cells and decreased hormone secretion. It was concluded that ergotamine had a direct inhibitory action on the GH3 cell tumour which was not mediated through the dopaminergic mechanisms.

Animals↗