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R. K. MEYER and C. E. McCORMACK

SUMMARY

Ovulation in immature rats induced by daily subcutaneous administration of sheep follicle-stimulating hormone (FSH) was prevented by appropriately timed injection of phenobarbitone or by exposure to continuous light. Progesterone produced ovulation in light-blocked rats and in rats kept in standard lighting which had received a non-ovulatory dose of FSH.

These findings are interpreted to mean that ovulation produced by these preparations of FSH was due to a release of ovulating hormone from the pituitary gland. It is suggested that slight luteinizing hormone activity in an FSH preparation produces ovulation by causing the secretion of progesterone which then facilitates the release of ovulating hormone from the pituitary gland.

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C. Wüster, F. Raue, C. Meyer, M. Bergmann, and R. Ziegler

ABSTRACT

In a cross-sectional study of 39 patients with medullary thyroid carcinoma (MTC), we have investigated the effects of long-term calcitonin excess on bone mineral density.

Bone mineral density was measured by dual X-ray absorptiometry at the lumbar spine between the second and fourth vertebra and by single photon absorptiometry at the distal forearm. The mean observation time of each patient between diagnosis of tumour and measurement of bone mineral density was 62·4 months (range 1–158 months). The mean calcitonin serum level was 14·4 μg/l at the time of measurement of bone mineral density. All patients were substituted with 150–200 μg l-thyroxine daily. At both sites, the mean bone mineral densities of all patients with MTC were not significantly different from controls. Patients with normal calcitonin levels (below 0·2 μg/l) after treatment had a normal bone mineral density of the spine but significantly (P <0·05) reduced bone mineral density values of the forearm. This was due to the decreased body surface areas of patients in this subgroup. Patients with multiple endocrine neoplasia type IIa had significantly higher bone mineral densities. Other bone-influencing factors, such as postoperative hypoparathyroidism, calcium intake, diarrhoea, menopause, tumour stage, previous anti-tumour treatment, or thyroxine substitution dose, did not affect bone mineral density.

We thus conclude that long-term excess of endogenous calcitonin in patients with MTC has no positive effect on bone mineral density.

Journal of Endocrinology (1992) 134, 141–147

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W. F. WARD, R. K. MEYER, and R. C. WOLF

SUMMARY

Rats were exposed to either 300 or 500 röntgen (R) acute whole-body X-irradiation on the 5th day of delayed pregnancy induced by ovariectomy. From 0 to 8 days after irradiation, implantation was induced by the administration of oestrogen. Foetal survival to the 20th day of development was used as an index of radiation effect.

If oestrogen was given immediately after exposure to 300 R, or 12 h later, only 30–35% of the embryos survived, significantly less (P < 0·01) than the non-irradiated control values of 74–79%. When implantation was postponed for 24 h or more, embryonic survival ranged from 57 to 64% and was not significantly different from that of controls.

After exposure to 500 R X-irradiation, embryonic survival increased linearly from 2% to a maximum of 41% as the interval between irradiation and oestrogen administration increased from 0 to 48 h. Embryonic survival never reached control levels after 500 R, regardless of the interval between irradiation and implantation. The irradiation regimens also induced developmental abnormalities, doubled the incidence of dead foetuses (death at a late stage of development), and significantly reduced foetal and placental weights at autopsy.

The results confirm that recovery from potentially lethal X-irradiation damage can occur during delayed implantation, and demonstrate that both the extent and the rate of recovery are functions of the radiation dose.

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C. Meyer, M. J. Freund-Mercier, Y. Guerné, and Ph. Richard

ABSTRACT

Plasma concentrations of oxytocin and vasopressin were measured in relationship to oxytocin cell firing during suckling in urethane-anaesthetized rats.

Preliminary experiments showed that plasma concentrations of oxytocin and vasopressin, which were increased immediately after anaesthesia, reverted to basal concentrations 3 h later. Moreover, it was found that exogenous oxytocin had entirely disappeared 5 min after i.v. bolus injections of known doses of oxytocin.

Suckling did not modify the basal plasma concentration of oxytocin (14·6 ± 2·9 compared with 14·±61·5 pmol/l before suckling) except during a brief period immediately after neurosecretory bursts on oxytocin cells (37·8 ± 5·2 pmol/l; P < 0·001, n = 11). The plasma concentration of oxytocin did not differ significantly from the basal concentration 1·5 min later. The plasma concentration of vasopressin never varied.

After two neurosecretory bursts of similar amplitude (total number of spikes during the burst) recorded on the same oxytocin cell, the variations in plasma concentration of oxytocin were also similar. When, for a given cell, the amplitude of neurosecretory bursts increased or decreased, the amount of oxytocin released changed in the same way.

These data demonstrate (1) that suckling induces pulsatile release of oxytocin without vasopressin, and (2) a direct relationship between the amounts of oxytocin released and the amplitude of oxytocin cell neurosecretory bursts which argue in favour of simultaneous increases or decreases in the neurosecretory burst amplitudes on all oxytocin cells.

J. Endocr. (1987) 114, 263–270

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C Voigt, HP Holzapfel, S Meyer, and R Paschke

G-protein-coupled receptor kinases (GRKs) are implicated in the pathophysiology of human diseases such as arterial hypertension, heart failure and rheumatoid arthritis. While G-protein-coupled receptor kinases 2 and 5 have been shown to be involved in the desensitization of the rat thyrotropin receptor (TSHR), their role in the pathophysiology of hyperfunctioning thyroid nodules (HTNs) is unknown. Therefore, we analyzed the expression pattern of the known GRKs in human thyroid tissue and investigated their function in the pathology of HTNs. The expression of different GRKs in human thyroid and HTNs was measured by Western blotting. The influence of GRK expression on TSHR function was analyzed by coexpression experiments in HEK 293 cells. We demonstrate that in addition to GRKs 2, 5 and 6, GRKs 3 and 4 are also expressed in the human thyroid. GRKs 2, 3, 5 and 6 are able to desensitize the TSHR in vitro. This GRK-induced desensitization is amplified by the additional over-expression of beta-arrestin 1 or 2. We did not find any mutations in the GRKs 2, 3 and 5 from 14 HTNs without TSHR mutations and Gsalpha mutations. The expression of GRKs 3 and 4 was increased in HTNs independently from the existence of TSHR mutations or Gsalpha mutations. In conclusion, the increased expression of GRK 3 in HTNs and the ability of GRK 3 to desensitize the TSHR in vitro, suggest a potential role for GRK 3 as a negative feedback regulator for the constitutively activated cAMP pathway in HTNs.

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B. Kacsoh, J. S. Meyers, W. R. Crowley, and C. E. Grosvenor

ABSTRACT

Serum GH levels increased in 2- or 8-day-old rat pups when sucking mammary glands whose main milk ducts were ligated. Although intragastric administration of rat milk has been shown to increase serum GH levels in neonatal rats, ingestion of milk during suckling did not increase serum GH values further. In another experiment, 2-day-old pups obtained no milk when they were suckled by anaesthetized mothers, and in this instance the serum GH concentration of the pups decreased. This decrease was prevented if the mothers were injected with oxytocin to counteract the depressant effect of the anaesthesia on milk ejection; nevertheless, GH levels in neonatal animals failed to increase following suckling. Thus some aspect of maternal activity appears to be involved in the suckling-induced increase of serum GH in rat pups. To elucidate which components of maternal activity might be involved, the effects of manipulations of ambient temperature as well as stimulation of the oral or anogenital regions were examined. Exposing rat pups to 37 °C (nest temperature) during the 6-h separation period before suckling prevented the separation-induced decrease in serum GH levels of 2-day-old pups. Moreover, exposure to 37 °C for 30 min following a 6-h separation at room temperature (22 °C) mimicked the effect of suckling in increasing serum GH levels in the pups. Suckling following separation at 37 °C was unable to increase serum GH values further. In other studies, stimulation of the oral zone (feeding from a soft cannula) or anogenital zone (inducing urination and defecation with a wet brush) of the pups significantly decreased neonatal serum GH values. The painful stimulus of administration of s.c. hyperosmotic saline was without effect on serum GH levels.

In summary: (1) suckling, even without milk removal, increases serum GH levels in neonatal rats; (2) some aspect of maternal activity is involved in the suckling-induced increase of serum GH concentration in the neonate; (3) provision of a warm ambient temperature by the mother is a critical component of this maternal activity; (4) the effects of milk and the maternal activity associated with suckling are not additive in increasing serum values of GH in neonatal rats; and (5) oral feeding is not a suitable approach for studying the effects of milk on serum GH in neonatal rats.

Journal of Endocrinology (1990) 124, 233–240

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Matthias R Meyer, Natalie C Fredette, Matthias Barton, and Eric R Prossnitz

Complications of atherosclerotic vascular disease, such as myocardial infarction and stroke, are the most common causes of death in postmenopausal women. Endogenous estrogens inhibit vascular inflammation-driven atherogenesis, a process that involves cyclooxygenase (COX)-derived vasoconstrictor prostanoids such as thromboxane A2. Here, we studied whether the G protein-coupled estrogen receptor (GPER) mediates estrogen-dependent inhibitory effects on prostanoid production and activity under pro-inflammatory conditions. Effects of estrogen on production of thromboxane A2 were determined in human endothelial cells stimulated by the pro-inflammatory cytokine tumour necrosis factor alpha (TNF-α). Moreover, Gper-deficient (Gper −/−) and WT mice were fed a pro-inflammatory diet and underwent ovariectomy or sham surgery to unmask the role of endogenous estrogens. Thereafter, contractions to acetylcholine-stimulated endothelial vasoconstrictor prostanoids and the thromboxane-prostanoid receptor agonist U46619 were recorded in isolated carotid arteries. In endothelial cells, TNF-α-stimulated thromboxane A2 production was inhibited by estrogen, an effect blocked by the GPER-selective antagonist G36. In ovary-intact mice, deletion of Gper increased prostanoid-dependent contractions by twofold. Ovariectomy also augmented prostanoid-dependent contractions by twofold in WT mice but had no additional effect in Gper −/− mice. These contractions were blocked by the COX inhibitor meclofenamate and unaffected by the nitric oxide synthase inhibitor l-NG-nitroarginine methyl ester. Vasoconstrictor responses to U46619 did not differ between groups, indicating intact signaling downstream of thromboxane-prostanoid receptor activation. In summary, under pro-inflammatory conditions, estrogen inhibits vasoconstrictor prostanoid production in endothelial cells and activity in intact arteries through GPER. Selective activation of GPER may therefore be considered as a novel strategy to treat increased prostanoid-dependent vasomotor tone or vascular disease in postmenopausal women.