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ABSTRACT
Neurohypophysial hormones stimulate gonadotrophin release from dispersed rat anterior pituitary cells in vitro, acting through receptors distinct from those which mediate the secretory response to gonadotrophin-releasing hormone (GnRH). The LH response to oxytocin was not affected by the presence of the phosphodiesterase inhibitor, methyl isobutylxanthine, but was diminished in the absence of extracellular calcium and was progressively increased as the calcium concentration in the medium was raised to normal. In addition, the calcium channel antagonist, nifedipine, suppressed oxytocin-stimulated secretion of LH. It is likely that the mechanisms of LH release induced by GnRH and neurohypophysial hormones are similar, although stimulation of gonadotrophin secretion is mediated by separate receptor systems. Oxytocin was more active than vasopressin in releasing LH, but less active in releasing ACTH. The highly selective oxytocin agonist, [Thr4,Gly7]oxytocin, elicited concentration-dependent secretion of LH but had little effect on corticotrophin secretion. The neurohypophysial hormone antagonist analogues, [d(CH2)5Tyr(Me)2]-vasopressin, [d(CH2)5Tyr(Me)2,Orn8]vasotocin and [d(CH2)5 d-Tyr(Et)2Val4,Cit8]vasopressin, inhibited the LH response to both oxytocin and vasopressin. However, [d(CH2)5Tyr(Me)2]vasopressin was much less effective in inhibiting the ACTH response to the neurohypophysial hormones, and [d(CH2)5Tyr-(Me)2,Orn8]vasotocin and [d(CH2)5 d-Tyr(Et)2,Val4, Cit8]vasopressin exhibited no inhibitory activity against ACTH release. Thus, agonist and antagonist analogues of neurophypophysial hormones display divergent activities with regard to LH and ACTH responses, and the neuropeptide receptor mediating gonadotroph activation is clearly different from that on the corticotroph. Whereas the corticotroph receptor is a vasopressin-type receptor an oxytocin-type receptor is responsible for gonadotrophin release by neurohypophysial hormones.
Journal of Endocrinology (1989) 122, 107–116
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ABSTRACT
Gonadotrophin-releasing activity of oxytocin has previously been demonstrated in vitro and in vivo. This study investigated whether oxytocin is also able to induce LH accumulation in pituitary cells. Following trypsin digestion and mechanical dispersion, pituitary cells from female rats were incubated with oxytocin (100 nmol/l) for 24 h. LH release stimulated by oxytocin increased (P < 0·001) progressively during the incubation indicating a different secretory pattern from the more rapid but less sustained secretion stimulated by gonadotrophin-releasing hormone. Oxytocin also enhanced (P < 0·01) total LH accumulation in the incubation system (released plus cell contents) which was apparent after 7–11 h of stimulation. The release of LH stimulated by oxytocin was reduced by the protein synthesis inhibitor cycloheximide (10 μmol/l). However, cycloheximide did not completely block oxytocin-stimulated LH release; there remained some LH release above that seen in non-stimulated controls (P < 0·01) revealing the presence of a cycloheximide-resistant component in the release mechanism. Furthermore, accumulation of total LH in 24 h incubations was suppressed (P < 0·01) by cycloheximide.
The advancement in LH release which oxytocin has been shown to induce in vivo in pro-oestrous rats was accompanied by an early reduction of pituitary LH stores. However, the fall normally observed in LH content during the surge was markedly attenuated by the oxytocin treatment. Thus, loss of pituitary LH stores was less in oxytocin-treated rats than in saline-treated controls, even though net LH release into plasma was increased. Therefore, oxytocin stimulated the replenishment of LH stores.
Although the mechanism(s) remains to be defined and the relationships between in-vitro and in-vivo results are as yet uncharacterized, the present study demonstrates that oxytocin treatment stimulates LH production in both dispersed cells and intact pituitaries in situ.
Journal of Endocrinology (1992) 132, 277–283
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ABSTRACT
Neurohypophysial hormones have been implicated in the control of anterior pituitary function, and oxytocin has been shown to stimulate gonadotrophin excretion and ovarian follicular development in certain species. To determine the role of neurohypophysial peptides in the control of gonadotrophin release, their actions on LH and FSH secretion were analysed in rats in vivo and in vitro. In adult female rats, administration of oxytocin during early pro-oestrus advanced the spontaneous LH surge and markedly increased peripheral LH levels at 15.00 h compared with control animals. In cultured pituitary cells from adult female rats, oxytocin and vasopressin elicited dose-related increases in LH and FSH release. Such responses were not affected by a potent gonadotrophin-releasing hormone (GnRH) antagonist that abolished GnRH agonist-induced release of LH and FSH. Oxytocin did not enhance GnRH agonist-stimulated gonadotrophin release to the same extent as it increased basal secretion, but at low concentrations of GnRH agonist the effects were additive. The gonadotrophin responses to oxytocin and vasopressin were inhibited by the specific neurohypophysial hormone antagonists, [d(CH2)5 d-Ile2,Ile4,Arg8]vasopressin and [d(CH2)5Tyr (Me),Arg8]vasopressin. These results provide direct evidence that neurohypophysial hormones can stimulate gonadotrophin secretion through a receptor system distinct from the GnRH receptor. Such a mechanism could represent a complementary hypothalamic control system for long-term modulation of LH and FSH secretion by exerting a basal or tonic influence on gonadotrophin production.
Journal of Endocrinology (1989) 122, 99–106
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SUMMARY
A procedure for extracting both gonadotrophin and growth hormone from acetone-dried pituitary powder in a form suitable for clinical use is described. Gonadotrophin is extracted first and fractionated by ethanolic precipitation; growth hormone is then extracted from the residues by a modification of Raben's procedure. The yields and potency of the products are given with particular emphasis on their activities in man. The economy of the preparation of gonadotrophin and growth hormone from human pituitaries is discussed.
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ABSTRACT
Considerable differences have previously been found in the hypothalamo-hypophysial responsiveness to oestrogen, depending upon the time between gonad removal and exposure to oestrogen. In the present study a detailed analysis was made of some of the differences which may exist in pituitary LH-releasing hormone (LHRH) receptors and the amount of LH released in response to electrochemical depolarization of the medial preoptic area after 2 or 7 days of oestradiol treatment of long- and short-term gonadectomized male and female rats. The pituitary glands of long-term gonadectomized males and females secreted more LH in response to two pulse injections of LHRH than did short-term gonadectomized rats. The amount of LH released on day 2, however, was equivalent to that secreted after 7 days of oestradiol treatment. Moreover, long-term gonadectomized males and females had equivalent LHRH receptor concentrations, which were greater than those of short-term gonadectomized animals. Peak serum LH concentrations observed after preoptic stimulation were equivalent in short- and long-term castrated rats after 2 days of oestrogen exposure. Serum LH concentrations following preoptic stimulation in short-term gonadectomized males and females were significantly greater on day 7 than on day 2 of oestradiol treatment, whereas in long-term gonadectomized animals the stimulated release of LH was equivalent both in magnitude and time of peak release on both days.
These studies demonstrate that the differential effects of oestradiol on LH release on day 2 (no negative feedback) compared with day 7 (both negative and positive feedback exist) are not due to differences in the ability of the pituitary gland to release LH in response to LHRH, nor in the releasable pools of hypothalamic LHRH in long-term gonadectomized rats. Rather, they seem to be due to a refractoriness in some unidentified central nervous process which regulates tonic LH release in gonadectomized rats.
J. Endocr. (1986) 110, 367–373
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Concentrations of human growth hormone (HGH) in pituitary tumours measured by the tibial line assay (Young, Bahn & Randall, 1965) or assessed visually from electrophoretic patterns of pituitary extracts (Lloyd & Meares, 1965) have been shown to vary from quite low levels to concentrations greater than those present in the normal anterior pituitary gland. In the present study, HGH concentration in four normal anterior pituitary glands, obtained at autopsy, and in six pituitary tumours, resected surgically, has been estimated by radioimmunoassay and by inspection of starch-gel electrophoresis patterns. Histological examination of the tumour tissue was performed on paraffin sections of formalin-fixed specimens after staining with haematoxylin and eosin, eosin and methyl blue, and PAS-orange G. Extracts of pituitary tissue were prepared by homogenization in tris-EDTA-boric acid buffer at pH 8·9. The clear supernatant obtained after centrifugation was subjected to radioimmunoassay and to starch-gel electrophoresis. Radioimmunoassay was performed by the solid-phase
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SUMMARY
Twenty-day-old male rats were injected intraperitoneally with either human luteinizing hormone (HLH) or human growth hormone (HGH) labelled with 125I. The localization of these hormones 1–2 hr. after injection was examined under the light microscope after radioautography.
Major sites of localization of labelled LH were the interstitial cells of the testis and the proximal convoluted tubule of the kidney. Some hormone was also present in adipose tissue, hepatic parenchymal cells, the mesothelial lining of the peritoneum and underlying macrophages. HGH was localized principally in the proximal convoluted tubule of the kidney with some hormone present in liver, adipose tissue, and the suprarenal cortex.