Vasopressin and vascular regulation: is sex a factor?
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Animals↗
Biomedical subjects
S A Whitehead
Publications and source records attributed to S A Whitehead.
Inhibitory action of peritoneal macrophages on progesterone secretion from co-cultured rat granulosa cells.
Resident ovarian macrophages are recognized as potential regulators of ovarian function, and the majority of evidence suggests that such regulation is mediated through cytokine secretions, particularly interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha). In this study we examine the effects of co-cultured macrophages, stimulation and inhibition of the immune system, and IL-1 beta and TNF alpha on gonadotropin-induced progesterone secretion from rat granulosa cells. Granulosa cells were isolated from ovarian follicles of proestrous rats and were cultured for a period of 48 h. Peritoneal macrophages, obtained from untreated rats or from animals pretreated with either thioglycollate (TG) or lipopolysaccharide (LPS), were plated at concentrations of 10(5), 5 x 10(3), or 2 x 10(3) cells/ml. After their adherence to the base of the culture wells, 1 ml of serum-free McCoy's medium containing 3 x 10(5) granulosa cells/ml were added to the macrophages. Gonadotropin-induced progesterone secretion was markedly inhibited in the co-cultures, and the degree of inhibition was dependent on both the number of co-cultured macrophages and whether or not the macrophages had been pre-activated by either TG or LPS. TG-activated macrophages were most potent in this respect. Such effects were not due to cytotoxic effects of the macrophages on granulosa cells as determined by a colorimetric assay for cellular growth and survival. In fact, macrophages increased the number of viable granulosa cells after 48-h culture. Granulosa cells obtained from animals pretreated with LPS showed a reduced ability to respond to ovine LH, although suppression of the immune system with cyclosporin had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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Effects of lipopolysaccharide and cyclosporin on the endocrine control of ovarian function.
The effects of stimulating the immune system with lipopolysaccharide (LPS) or suppressing the immune system with cyclosporin (CS) on reproductive functions in the female rat were investigated. Animals were either treated acutely with LPS (2 mg kg-1) or cyclosporin (20 mg kg-1) on dioestrus day 1 and 2 or treated chronically over a period of 6 days (on alternate days with LPS, daily with CS). Chronic LPS treatment induced a state of constant dioestrus and decreased circulating concentrations of progesterone and oestradiol. Chronic CS treatment induced some irregularity in the 4-day vaginal smear pattern in a minority of animals and, while it had no effect on circulating concentrations of progesterone, oestradiol concentrations were suppressed compared with those measured in pro-oestrous animals. LH responses to GnRH were reduced in both perifused pituitary fragments and cultured pituitary cells obtained from animals pretreated with either LPS or CS. In contrast, a low dose of LPS (20 micrograms kg-1) given over 6 days did not disrupt ovarian cycles and reduced, but did not abolish, the second phase primed LH response. Neither drug had a direct effect on the pituitary LH responses to GnRH, except that pituitary cells exposed to high doses of CS for periods greater than 48 h did show attenuated LH responses to GnRH. This finding was not paralleled with high doses of LPS. The differential count of ovarian follicles from histological studies showed that LPS treatment was associated with significantly fewer large preovulatory follicles, whereas animals treated with CS showed a similar distribution of follicular volumes compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Restorative decision-making behavior with magnification.
Assessment of occlusal fissure systems and restorations of amalgam in 100 extracted teeth were carried out by four examiners. An initial assessment, made with the naked eye, was repeated with binocular magnification (x 3). The data indicated that restorative decision-making behavior was modified when magnification was used, with an increase in the number of restorations planned for replacement and an increase in the number of tooth surfaces planned for restoration. Statistical analysis indicated that one of the examiners was particularly sensitive to the use of magnification and modified his treatment planning behavior considerably. As part of the process of adapting to the use of magnification, clinicians should review their decision-making behavior.
Decision Making↗
Demonstration of a nonsteroidal factor in human follicular fluid that attenuates the self-priming action of gonadotropin-releasing hormone on pituitary gonadotropes.
The self-priming effect of gonadotropin-releasing hormone (GnRH) on luteinizing hormone (LH) release can be demonstrated in vitro by perfusing pituitary tissue with a continuous GnRH stimulus. A characteristic biphasic response is produced. We have used this system to investigate whether or not human follicular fluid (hFF) contains a nonsteroidal substance that can attenuate the GnRH-induced LH secretion in perfused rat pituitary glands. Steroid-extracted hFF, added to the perfusing medium, attenuated the self-priming action of GnRH in a dose-dependent manner. This was not abolished by selectively depleting the inhibin content of hFF by 97% on an immunoaffinity column. Furthermore, the biological activity of the substance was resistant to heating and was removed by dialysis. It is concluded that hFF contains a nonsteroidal factor, distinct from inhibin, that can attenuate the self-priming action of GnRH on pituitary gonadotropes.
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Non-steroidal follicular factors attenuate the self-priming action of gonadotropin-releasing hormone on the pituitary gonadotroph.
Pituitary glands of pro-oestrous and oestrous rats were perifused in series with isolated ovarian follicles and the luteinizing hormone (LH) and follicle-stimulating hormone (FSH) responses to gonadotropin-releasing hormone (GnRH) were measured. Pituitary glands from pro-oestrous rats, perifused with the effluent medium from isolated preovulatory follicles, showed a significant reduction in the self-priming effect of GnRH as observed from the typical biphasic LH response to a continuous GnRH challenge. The initial FSH response to GnRH was also reduced. A similar trend was seen in the LH responses of pituitary glands from oestrous rats but results were not significant; there was no parallel reduction in FSH release. It is unlikely that the attenuation of GnRH self-priming was due to the steroids released by the isolated follicles. LH responses of pro-oestrous pituitaries, perifused with medium containing 200 pg oestradiol/ml, 5 ng progesterone/ml or 200 pg testosterone/ml were similar to paired controls as were the responses when all three steroids were added to the perifusing media at identical concentrations. Furthermore, when steroids were charcoal extracted from the effluent medium of perifused isolated follicles the biological activity of this medium in attenuating GnRH self-priming was not destroyed. Finally, the effects of purified bovine inhibin and steroid-free human follicular fluid (hFF) on LH responses were compared. Purified inhibin at a concentration of 20 or 50 ng/ml perifusing medium had no effect on GnRH-stimulated LH release although GnRH-stimulated FSH secretion was significantly reduced toward the end of an extended perifusing period.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A gonadotrophin surge attenuating factor?
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Animals↗
Effects of approximal finishing strips.
The effects of a representative sample of approximal finishing strips on the surfaces of restorations, the approximal margins of restorations and on the surfaces of enamel adjacent to restorations have been evaluated using scanning electron microscopy. The results indicate that the sample of finishing strips investigated tend to damage the surface of enamel and fail to leave restorations with either ideal surface finish or marginal adaptation. Guidelines are suggested for the choice of approximal finishing strips in selected clinical situations.
Dental Bonding↗
The nature and effects of composite finishing pastes.
Specimens of composite resins, contoured and finished with a series of microfine diamonds, were finished with a selection of commercially available composite finishing pastes. The resulting surfaces were examined using scanning electron microscopy (SEM) and surface profilometry. Samples of the pastes were investigated using SEM and energy dispersive X-ray spectroscopy. All the paste systems employed an abrasive of similar composition and particle size. The selection of finishing pastes produced marked improvements of the surfaces of the composite resins. The small differences measured between the performances of the four finishing pastes included in this study could not be corroborated by SEM evaluation. Therefore, within the limitations of this study, there was little evidence to suggest that any one paste system was superior to the others. The results of this study indicate that commercially available composite resin finishing pastes of the type investigated may be used to improve the surface of all types of contemporary composite resins and may be of particular value in finishing the concave surfaces of restorations of composite resins following contouring and finishing with microfine diamond burs.
Composite Resins↗
Effects of ovarian hyperstimulation and isolated preovulatory follicles on LH responses to GnRH in rats.
Adult rats were pretreated with a 3-day regimen of human menopausal gonadotrophin (hMG), PMSG, human FSH or hCG and experiments were carried out on the day of pro-oestrus. Treatment with hMG and hFSH induced a significant increase in the number of preovulatory follicles on the day of pro-oestrus and this was correlated with increased circulating concentrations of oestradiol. There was a parallel increase in the self-priming effect of GnRH, as observed from the biphasic LH response to a continuous GnRH challenge. PMSG treatment did not stimulate increased numbers of maturing follicles and was less effective in raising circulating oestrogen concentrations compared with hMG and hFSH. However, pituitary responsiveness was much higher after PMSG treatment and the biphasic response to continuous perfusion with GnRH was absent; LH release was high from the initiation of the stimulus. hCG alone failed to stimulate follicular maturation but enhanced pituitary LH responses. Hemi-pituitary glands perfused in the presence of isolated preovulatory follicles also showed augmented biphasic LH responses to GnRH compared with control hemi-pituitary glands. The apparent dissociation which can occur between follicular maturation, circulating oestrogen concentrations and pituitary responsiveness to GnRH supports the idea of non-steroidal ovarian factors modulating LH release.
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Increased responsiveness of the hypothalamic-pituitary axis to steroid feedback effects in ovariectomized rats treated neonatally with monosodium L-glutamate.
Chronic ovariectomized rats treated neonatally with MSG showed reduced circulating concentrations of LH coupled with elevated hypothalamic LHRH stores. Despite the apparent loss of LHRH secretion, the small pituitary glands showed an increased density of LHRH receptors and normal responsiveness to the releasing hormone. The positive feedback effects of progesterone on LH release in oestrogen-primed animals was greatly exaggerated reflecting the build-up of hypothalamic LHRH stores without loss of pituitary responsiveness to LHRH.
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Feedback effects of gonadal steroids and pituitary LH-releasing hormone receptors in the streptozotocin-induced diabetic rat.
The effects of streptozotocin (STZ)-induced diabetes mellitus on the positive feedback action of steroids on luteinizing hormone (LH) secretion have been investigated in the oestrogen-primed ovariectomized rat. Rats treated with 40 mg/kg STZ 2 weeks before experimentation showed an attenuated LH surge in response to progesterone, an effect only partially restored by insulin replacement. When the same dose of the drug was injected just 24 h before the progesterone treatment it had no effect on the LH surge, while a high dose of 80 mg/kg STZ completely abolished the positive feedback action of the steroid. Insulin treatment did not reverse this effect. In parallel the effects of 2-week and 24-h diabetes on pituitary LH-releasing hormone (LRH) receptors were studied. Pituitary binding of a long acting LRH analogue was reduced in the 2-week diabetic animals, although a more dramatic reduction was observed in the rats treated with the high dose of STZ 24 h before testing. The results suggest that diabetes impairs the positive feedback effects of gonadal steroids resulting in a reduced release of LRH. However, the impairment is unlikely to be caused simply by hyperglycaemia but by non-specific toxic side effects of STZ and/or other metabolic changes associated with diabetes.
Animals↗
A comparison of the effects of gonadal steroids on naloxone-induced LH secretion in gonadectomized rats.
The effects of the opiate antagonist naloxone on serum LH concentrations was investigated in gonadectomized rats given different regimes of steroid pretreatment. Two injections of testosterone given 48 and 24 h before naloxone treatment failed to reinstate LH responses to this drug in castrated rats while subcutaneous testosterone-filled silicone elastomer capsules implanted for a week were effective in this respect. Injections of oestrogen, oestrogen plus progesterone or progesterone alone all restored LH responses to naloxone in ovariectomized rats when given 48 and/or 24 h before drug treatment, although the magnitude of these responses varied according to the precise steroid treatments. The hypothalamic-pituitary axis was also responsive to naloxone just before the progesterone-induced LH surge in oestrogen-primed ovariectomized rats. Results show that gonadal steroids are permissive to the effects of opiate drugs, but they suggest that endogenous opioid systems do not necessarily mediate the negative feedback effects of steroids. Some other factor(s), as yet unidentified in the rat, may control the opioid modulation of gonadotrophin secretion or exert an independent inhibitory effect on gonadotrophin release.
Animals↗
Feedback effects of steroids and gonadotrophin control in adult rats with streptozotocin-induced diabetes mellitus.
The effects of long-and short-term streptozotocin-induced diabetes mellitus on the control of gonadotrophin secretion have been investigated in adult intact rats. A high dose of streptozotocin (80 mg/kg), administered intraperitoneally 3 days before experimentation, inhibited ovulation and reduced the pituitary luteinizing hormone response to luteinizing hormone releasing hormone in proestrous rats. A lower dose (40 mg/kg) did not inhibit ovulation but abolished the luteinizing hormone releasing hormone-priming effect on the pituitary which normally occurs on proestrus, prior to ovulation. Oestrous cyclicity was lost when diabetes was induced for 14 or 56 days, but there was no effect on pituitary responsiveness to luteinizing hormone-releasing hormone compared with control animals. Similar observations were made with rats placed on a food-restricted diet. In all experiments there was no difference between diabetic and control animals in the pituitary luteinizing hormone content, the hypothalamic content of luteinizing hormone-releasing hormone or the ovarian weights. Ovariectomized rats treated with streptozotocin (40 mg/kg) were used to investigate the effects of diabetes on steroid feedback mechanisms. There was an attenuated luteinizing hormone response to ovariectomy in diabetic compared with control animals, and an impaired positive feedback effect of progesterone in oestrogen-primed animals. The results show that streptozotocin-induced diabetes mellitus inhibits feedback action of gonadal steroids and this could account for both the loss of oestrous cyclicity and the reduced pituitary sensitivity to luteinizing hormone-releasing hormone.
Animals↗
Changes in pituitary responsiveness to LH-releasing hormone after acute buserelin treatment: a time-course and dose-response study.
The acute in-vivo effects of a potent LH-releasing hormone (LHRH) agonist, buserelin, on LH secretion and pituitary responsiveness to LHRH have been investigated in oestrous rats. Doses of 50, 100 and 250 ng buserelin stimulated LH release in a dose-dependent manner, the peak serum LH concentrations being measured 1 h after the treatment. Thereafter LH levels fell rapidly between 1 and 6 h and by 18 h serum LH concentrations were similar in all groups of animals. Pituitary responsiveness to a challenge with 100 ng LHRH was potentiated by 50 or 100 ng buserelin injected 1 or 2 h before the LHRH challenge. In contrast, 250 ng buserelin completely abolished the LH response to LHRH when tested 1, 2 and 4 h after treatment, but by 6 h a small but attenuated response was observed. Four hours after treatment there was no significant difference in the responses when compared with the saline-treated controls.
Animals↗
Pituitary receptors for LH-releasing hormone (LHRH) and responsiveness to LHRH in adult female rats after neonatal monosodium L-glutamate treatment.
The effects of neonatal monosodium L-glutamate (MSG) treatment on pituitary responsiveness to LH-releasing hormone (LHRH) and on pituitary LHRH receptors have been investigated in the intact adult female rat. Three- to four-month-old rats treated with MSG (4 mg/g body wt) on days 2, 4, 6, 8 and 10 after birth had significantly reduced ovarian and pituitary weights, showed an absence or disruption of ovarian cyclicity after puberty, and had significantly higher concentrations of serum prolactin despite normal levels of LH. In-vitro pituitary LH responses to LHRH were in the normal range for one group of treated animals whilst in a second group the LH responses were markedly enhanced. In contrast, the total number of pituitary LHRH receptors were significantly reduced in all MSG-treated animals showing that the increased pituitary responsiveness of MSG-treated animals is not attributable to an increase in pituitary LHRH receptors.
Animals↗
Effects of 6-hydroxydopamine treatment of rats on the in-vitro release of LHRH and pituitary responsiveness to LHRH.
Injection of 150 micrograms 6-hydroxydopamine (6-OHDA) into the third ventricle of rats depleted the mean hypothalamic concentration of noradrenaline by 71% whereas the mean dopamine concentration was only reduced by an insignificant 7%. Isolated perfused pituitary glands taken from intact 6-OHDA-treated rats showed a markedly increased LH response to pulses of LHRH although there was no significant difference in the circulating levels of LH. Ovarian cyclicity was disrupted and the hypothalamic content of LHRH was significantly reduced. Hypothalamic synaptosomes prepared from intact 6-OHDA-treated animals consistently released less LHRH than did controls although the difference was not significant. Noradrenaline, dopamine and adrenaline did not significantly affect LHRH release from experimental or control synaptosome preparations. In ovariectomized rats 6-OHDA treatment did not inhibit the positive feedback effects of progesterone administration to oestrogen-primed animals, although the negative feedback effects of the priming oestrogen treatment was augmented. The results indicate that depletion of hypothalamic noradrenaline causes subtle changes in the endogenous release of LHRH and may alter the negative feedback effects of steroids on the hypothalamic-pituitary axis.
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Evidence for an increased opioid inhibition of LH secretion in hyperprolactinaemic ovariectomized rats.
The effects of acute and sub-chronic hyperprolactinaemia on the positive feedback action of progesterone in oestrogen-primed ovariectomized rats have been compared. A single injection of ovine prolactin administered with progesterone had no effect on the LH surge measured 5 h later although hyperprolactinaemia induced by 5-day treatment with the dopamine antagonist, domperidone, markedly attenuated the surge. Repeated injections of naloxone (5 mg/kg) during the development of the progesterone-stimulated LH surge completely reversed this inhibitory effect of hyperprolactinaemia, but had no apparent effect on the positive feedback action in control animals. In oestrogen-primed animals similar treatment with naloxone (0.4 and 5 mg/kg) stimulated LH secretion but the increase was significantly smaller than that observed after injecting progesterone. It is suggested that hyperprolactinaemia increases the inhibitory opioid modulation of LH release and that this effect is responsible for the impairment of the positive feedback action of progesterone.
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