Sexually dependent changes in rat somatotropic cells following bilateral adrenalectomy.

In order to elucidate the existence of gender-related variations in both growth hormone (GH) release and the activity of somatotropic cells following bilateral adrenalectomy, a morphometric analysis was performed on GH-immunoreactive cells from adult male and female rats after bilateral adrenalectomy, correlating the findings with the serum levels of the hormone. The results obtained were compared to those found in untreated animals. Bilateral adrenalectomy was seen to induce a decrease in serum GH levels (p less than 0.01) in male rats; this was accompanied by a significant decrease in cellular area (p less than 0.01), cytoplasmic area (p less than 0.05) and nuclear area (p less than 0.01) and by a decrease in the cytoplasmic immunoreaction intensity of GH cells. By contrast, the above-mentioned changes did not appear in the female rats. These results suggest that the action of glucocorticoids on the synthesis and release of GH depends on the sex of the animal.     

The influence of ovarian factors on the somatostatin-growth hormone system during the postnatal growth and sexual development in lambs

The aim of the study was to elucidate the effects of ovarian hormones on somatostatin in the hypothalamic neurons and growth hormone (GH) secretion during the postnatal growth and development of sheep. The study was performed on 9-week-old (infantile) lambs that were ovary-intact (OVI) or ovariectomized (OVX) at 39 days of age, and on 16-week-old (juvenile) lambs that were OVI or OVX at 88 days of age. Hormones in neurons and somatotropic cells were assayed with immunohistochemistry and radioimmunoassay. Following ovariectomy, immunoreactive somatostatin was more abundant (p<0.05) in the hypothalamus of infantile lambs, whereas in juvenile lambs it was more abundant (p<0.05) in the periventricular nucleus but reduced (p<0.01) in the median eminence. In contrast to somatostatin in the hypothalamus, the content of immunoreactive GH in the hypophysis was less in OVX infantile lambs, but greater in OVX juvenile lambs (p<0.05). Basal blood serum concentrations of GH were greater (p<0.05) in OVX infantile lambs, whereas in OVX juvenile lambs, mean and basal concentrations of GH and amplitude of GH pulses were less than in OVI lambs (p<0.05). The postnatal increase in body weight was greatest in middle-late infancy (p<0.01). The body weight did not differ (p>0.05) between OVI and OVX lambs. In conclusion, ovarian factors may inhibit the GH secretion in infantile lambs but enhance the GH secretion in juvenile lambs. Transition to puberty, as related to the growth rate, appears to be due mainly to change in gonadal influence on the somatostatin neurosecretion. A stimulation of somatostatin output in the median eminence by gonadal factors in infancy is followed by a stimulation of somatostatin accumulation after infancy. Thus, ovarian factors modulate mechanisms within the somatotropic system of lambs to synchronize the somatic growth with sexual development.     

Morphometric changes in GH-immunoreactive adenohypophyseal cells induced by intraventricular administration of colchicine to adult rats.

In order to elucidate whether the gender differences observed in the somatotropic cells of adult rats are mediated by hypothalamic neuropeptides, a morphometric analysis was made of the GH-immunoreactive cells of adult rats treated intraventricularly with colchicine. The morphometric and morphological findings obtained were correlated to the basal serum levels of GH at the time of sacrifice. Treatment with colchicine was seen to increase serum GH levels; this increase was accompanied by an increase in the intensity of the reaction of the GH-cells and, morphometrically, an increase in their size due to an increase in the nuclear area, but with no significant changes in the cytoplasmic area. The results suggest that in the absence of somatostatin and GRF the basal release of GH is elevated in a similar fashion in both sexes, in turn suggesting that gonadal steroids might act at hypothalamic level on the release of somatostatin and, indirectly, on the intracellular pool of GH and hormonal secretion.     

Acute effects of unilateral sectioning the superior ovarian nerve of rats with unilateral ovariectomy on ovarian hormones (progesterone,testosterone and estradiol) levels vary during the estrous cycle

The present study analyzed the participation of the left and right superior ovarian nerves (SON) in regulating progesterone, testosterone, and estradiol serum levels in unilaterally ovariectomized rats on each day of the estrous cycle. For this purpose, ovarian hormone concentrations in serum were measured in animals with either sham-surgery, unilateral ovariectomy (ULO), unilateral sectioning of the SON, or sectioning of the SON innervation of the in situ ovary in rats with ULO.     

Evaluation of the role of calcitonin deficiency in ovariectomy-induced osteopenia

Studies were carried out in rats to examine the role of calcitonin deficiency in the pathogenesis of ovariectomy-induced osteopenia. The parathyroid glands of 80 female Wistar rats were autotransplanted to their thigh muscle and the animals divided into 4 groups. Group 1 rats were sham ovariectomized, and thyroidectomized to make them calcitonin deficient; Group 2 rats were thyroidectomized, and ovariectomized to make them deficient in ovarian hormones as well; Group 3 rats were sham thyroidectomized and sham ovariectomized, and Group 4 rats were sham thyroidectomized and ovariectomized. A fifth group of rats were unoperated upon and served as controls. Thyroidectomized animals were maintained on thyroxine replacement and 11 months after ovariectomy all the animals were bled, killed and their femurs dissected out. In both the thyroid intact and thyroidectomized animals, ovariectomy decreased femur density significantly (P less than 0.01). Similarly, ovariectomy resulted in a decrease in femur calcium (P less than 0.01) in both groups of animals, and in a significant decrease in serum calcitonin (P less than 0.05) in the thyroid intact animals. We conclude from these findings that ovarian hormone deficiency can cause bone loss independently of lowering circulating calcitonin levels.     

Ovariectomy during the luteal phase influences secretion of prolactin, growth hormone, and insulin-like growth factor-I in the bitch

A decline in circulating progesterone concentration plays an important role in the ethiopathogenesis of pseudopregnancy in the bitch. Because growth hormone (GH) and prolactin (PRL) are essential for normal mammogenesis and the secretion of these hormones is influenced by changes in the circulating progesterone concentration, the purpose of this study was to investigate the effects of mid-luteal phase ovariectomy on the 6-h pulsatile plasma profiles of GH and PRL and the basal plasma concentrations of GH, PRL, and insulin-like growth factor-I (IGF-I) in six beagle bitches. Ovariectomy was followed by only mild or covert signs of pseudopregnancy. The sharp decrease of the plasma progesterone concentration was accompanied by decreased basal plasma concentrations of GH and IGF-I and a rise in basal plasma PRL concentration. GH and PRL were secreted in a pulsatile fashion both prior to and after ovariectomy. The mean basal plasma GH concentration was significantly higher before ovariectomy than on days 1 and 7 after ovariectomy. The mean area under the curve above the zero level (AUC(0)) for GH was significantly higher before than at 7 days after ovariectomy. The mean area under the curve above basal level (AUC(b)) and the frequency of GH pulses at 7 days after ovariectomy were significantly higher than before and 1 day after ovariectomy. Both the mean basal plasma PRL concentration and the mean AUC(0) for PRL increased after ovariectomy. In conclusion, ovariectomy of bitches in the mid-luteal phase stops progesterone-induced GH release from the mammary gland, as evidenced by the lowering of basal plasma GH levels, the recurrence of GH pulsatility, and the lowering of circulating IGF-I levels. The sudden lowering of plasma progesterone concentration is probably a primary cause of a prolonged increase in PRL secretion. These observations underscore the importance of similar, albeit less abrupt, hormonal changes in the cyclical physiological alterations in the mammary gland and in the development of pseudopregnancy.     

Effects of acute ovariectomy on anterior pituitary gland follicle-stimulating hormone and luteinizing hormone secretion in the metestrous rat

Changes at the anterior pituitary gland level which result in follicle-stimulating hormone (FSH) release after ovariectomy in metestrous rats were investigated. Experimental rats were ovariectomized at 0900 h of metestrus and decapitated at 1000, 1100, 1300, 1500, 1700 or 1900 h of metestrus. Controls consisted of untreated rats killed at 0900 or 1700 h and rats sham ovariectomized at 0900 h and killed at 1700 h. Trunk blood was collected and the serum assayed for FSH and luteinizing hormone (LH) concentrations. The anterior pituitary gland was bisected. One-half was used to assay for FSH concentration. The other half was placed in culture medium for a 30-min preincubation and then placed in fresh medium for a 2-h incubation (basal FSH and LH release rates). The basal FSH release rate and the serum FSH concentration rose significantly by 4 h postovariectomy and remained high for an additional 6 h. The basal FSH release rate and the serum FSH concentration correlated positively (r=0.71 with 72 degrees of freedom) and did not change between 0900 and 1700 h in untreated or sham-ovariectomized rats. In contrast, the serum LH concentration and the basal LH release rate did not increase after ovariectomy. Ovariectomy had no significant effect on anterior pituitary gland FSH concentration. The results suggest that the postovariectomy rise in serum FSH concentration is the result, at least in part, of changes which cause an increase in the basal FSH secretion rate (secretion independent of the immediate presence of any hormones of nonanterior pituitary gland origin). The similarities between the selective rises in the basal FSH release rate and the serum FSH concentration in the ovariectomized metestrous rat and in the cyclic rat during late proestrus and estrus raise the possibility that an increase in the basal FSH release rate may be involved in many or all situations in which serum FSH concentration rises independently of LH.     

尼尔雌醇对去卵巢大鼠骨元素代谢和相关激素含量的影响

目的：测定犬鼠骨矿物元素含量和血清相关激素及IL-6含量,研究尼尔雌醇（CCE3）对去卵巢（OVX）大鼠骨元素代谢和相关激素含量的影响。方法：健康4月龄雌性SD大鼠24只随机分成4组（n=6）：正常对照组;假手术组;去卵巢组;去卵巢＋CCE3组。去卵巢＋CCE3组大鼠于去卵巢手术后第2天开始给予CCE3灌胃,1ms／ks体重,每周1次,持续11周。结果：去卵巢组大鼠骨Ca、Mg、S、Co、Mn、Zn等元素含量显著降低,骨P（磷）含量升高,血清岛、P（孕酮）、TSH、T4、CT、Cortisol、GH等含量显著降低,IL-6、FSH、LH等含量显著升高。CCE3可使去卵巢大鼠骨Ca、Mg、Co、Mn、S、Zn等含量回升,骨P（磷）含量回降,血清E2、P（孕酮）、TSH、T4、CT、Cortisol、GH等显著回升,IL-6、FSH、LH等含量显著回降。结论：CCE3可纠正去卵巢所致的骨元素代谢紊乱,CCE3改变去卵巢大鼠体内相关激素和IL-6水平是CCE3去卵巢大鼠骨元素代谢紊乱的重要机制。     

The role of estrogen in the feedback regulation of follicle-stimulating hormone secretion in the female rat

Letrozole (CGS 20267) is a non-steroidal aromatase inhibitor which, at its maximally effective dose of 1 mg/kg p.o., elicits endocrine effects equivalent to those seen after ovariectomy. Adult, female cyclic rats were administered letrozole (1 mg/kg p.o.) once daily for 14 days. A control group of animals was ovariectomized on day 1 of treatment and a third group of animals served as untreated controls. During the experiment, vaginal smears were taken daily and at the end of 14 days all animals were sacrificed, trunk blood was taken for serum estradiol, LH and FSH measurements and the uterus and ovaries were removed and weighed. The ovaries were then fixed and prepared for histological examination. Serum hormone measurements showed that after treatment with letrozole, serum estradiol levels were reduced by 76% of untreated controls and serum LH was elevated to 378% of control values. These compared favorably with those seen after ovariectomy, serum estradiol was reduced by 78% and serum LH was elevated to 485% of untreated controls. However, FSH was unchanged after letrozole treatment (125% of control), whereas after ovariectomy FSH rose to 398% of control. Uterine weight was suppressed in the letrozole-treated animals as well as the ovariectomized animals by 60 and 70%, respectively. The histology of the ovaries of animals treated with letrozole were consistent with the serum hormone findings. Except for the effects on serum FSH, these results confirm previous findings that treatment with letrozole elicits endocrine effects similar to those seen after ovariectomy. Furthermore, these results demonstrate that FSH secretion is not under the control of estradiol whereas LH secretion is under feedback control of ovarian estrogen.     

Ovariectomy causes cell proliferation and matrix synthesis in the growth plate cartilage of the adult rat

The in vivo effects of ovariectomy in rats have been studied on cell proliferation and matrix synthesis in the growth plate cartilage by assessing immunohistochemically the levels of proliferating cell nuclear antigen and chondroitin sulphate proteoglycan(s). The serum levels of insulin-like growth factor-I and growth hormone were also measured by radioimmunoassay procedures. At 5 weeks after ovariectomy, the serum levels of the growth factor were significantly higher than those in sham-operated rats. In contrast, the level of growth hormone was lower. The nuclear staining of proliferating cell nuclear antigen was generally seen in the zone of proliferative chondrocytes from both groups of rats. Whereas almost all chondrocytes in the proliferative zone of ovariectomized rats expressed proliferating cell nuclear antigen immunoreactivity, fewer did so in that of the sham rats. Quantitative image analysis by ACAS 570 laser cytometry demonstrated that the n uclear antigen-positive sites in ovariectomized rats had significantly higher integrated values (staining intensity), areas and perimeters than those in sham rats. In addition, the number of chondroitin sulphate proteoglycan-immunoreactive cells in the proliferative chondrocytes was also higher in ovariectomized rats than in sham ones. These results suggest that ovariectomy significantly stimulates the cell proliferation and matrix synthesis in the growth plate cartilage, probably through the higher serum level of insulin-like growth factor-I.     

Hormone Therapy Alters the Composition of the Vaginal Microflora in Ovariectomized Rats

The aim of the present study was to evaluate the alterations that may take place in the bacterial genital tract flora in the absence of ovarian hormones. The role of hormone replacement therapy was also assessed. For this purpose, various bacteria were identified from the vaginal flora of ovariectomized and sham operated female rats, following the Bergey’s manual criteria. The data of this study showed that substantial differences exist in the vaginal bacterial microflora between ovariectomized and normal cyclic rats. Ovariectomy was associated with a lower total bacterial load that may be due mainly to the absence of Lactobacillus. Anaerobic bacteria were also absent. Streptococcus and Enterococcus were also not favored in an environment lacking the ovarian hormones. In contrast, C. perfringens, Bacteroides, S. epidermidis, and S. aureus were detected in high numbers in ovariectomized rats. In terms of the impact of hormone replacement therapy on vaginal flora, only estradiol (EE2) restored Lactobacillus levels in ovariectomized rats, whereas all hormonal schemes used brought Streptococcus, Clostridium lec (−), and C. perfringens, the spore and vegetative forms, close to those detected in normal cyclic female rats. In conclusion, ovarian hormones appeared to be regulatory factors that favor the presence of a broad variety of bacteria, which are members of the normal genital tract flora. On the other hand, ovariectomy modifies the vaginal microbial profile, and hormone replacement therapy based mainly on schemes containing EE2 could alleviate this disturbance.     

Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release

Growth hormone (GH) regulates whole body metabolism, and physical exercise is the most potent stimulus to induce its secretion in humans. The mechanisms underlying GH secretion after exercise remain to be defined. The aim of this study was to elucidate the role of estrogen and pituitary type 1 deiodinase (D1) activation on exercise-induced GH secretion. Ten days after bilateral ovariectomy, animals were submitted to 20 min of treadmill exercise at 75% of maximum aerobic capacity and tissues were harvested immediately or 30 min after exercise. Non-exercised animals were used as controls. A significant increase in D1 activity occurred immediately after exercise (~60%) in sham-operated animals and GH was higher (~6-fold) 30 min after exercise. Estrogen deficient rats exhibited basal levels of GH and D1 activity comparable to those found in control rats. However, after exercise both D1 activity and serum GH levels were blunted compared to sedentary rats. To understand the potential cause-effect of D1 activation in exercise-induced GH release, we pharmacologically blocked D1 activity by propylthiouracil (PTU) injection into intact rats and submitted them to the acute exercise session. D1 inhibition blocked exercise-induced GH secretion, although basal levels were unaltered. In conclusion, estrogen deficiency impairs the induction of thyroid hormone activating enzyme D1 in the pituitary, and GH release by acute exercise. Also, acute D1 activation is essential for exercise-induced GH response.     

Estradiol increases somatomedin-C concentrations in adolescent rhesus macaques (Macaca mulatta)

Estradiol (E2) may enhance somatomedin-C (Sm-C) secretion during puberty in female rhesus monkeys. The present study evaluated the importance of age and acute changes in E2 on Sm-C secretion. Intact (INT) females at their first ovulation (age 3.5 yr; n = 6) had higher levels of Sm-C across the ovulatory cycle than did intact adults (ADT) (n = 5). Levels of Sm-C were similar for both groups during the follicular and luteal phases despite higher follicular phase levels of E2. Young, ovariectomized, E2-treated (E2OVX) females (age 3.5 yr; n = 5; E2 = 50 pg/ml) had higher basal levels of Sm-C than did either age-matched ovariectomized (OVX) females (n = 3), ovariectomized adults (OXA), or E2-treated ovariectomized adults (E2A) (E2 = 100 pg/ml). When ovariectomized groups were given E2 to induce ovulatory increases, no changes in serum Sm-C occurred. Comparisons among age-mates revealed that basal levels of Sm-C were similar between INT and E2OVX, yet these levels were higher than those for OVX. Sm-C levels were similar among all adult groups. Serum growth hormone (GH) was highest in E2OVX, next highest in INT and OVX, and lowest in all adults. Higher Sm-C levels in young animals are, thus, related to these age differences in GH concentrations and are further enhanced by basal levels of E2 and not by acute changes in this steroid. Low Sm-C secretion in adults is associated with low GH levels. Thus, the facilitory effect of basal E2 on Sm-C release is observed during conditions when basal GH levels are elevated, a situation normally limited to adolescence.     

Profile of serum IL-1beta and IL-10 shortly after ovariectomy and estradiol replacement in rats

Ovariectomy leads to progressive and significant increases in body weight gain and osteoporosis and is related to changes in serum and tissue cytokine profiles, such as observed in other models of overweight. We aimed to evaluate serum interleukin-1beta and interleukin-10 shortly after ovariectomy, before the establishment of overweight in rats. Female Wistar rats were submitted to ovariectomy, ovariectomy and estradiol replacement, or sham operation and compared with intact controls. Rats were killed 3, 6, 9, or 13 d after ovariectomy. Body mass and retroperitoneal fats were significant higher only 13 d after ovariectomy, and estradiol replacement to ovariectomized rats impaired both body mass and retroperitoneal fat gain. Shortly after ovariectomy (at 3 d) serum interleukin-1beta levels significantly increased in ovariectomized rats, treated or not with estradiol, while serum interleukin-10 levels increased only 9 d after ovariectomy. Our results suggest the existence of an important interplay between the immune system and ovarian function. This interplay occurs regardless of significant changes in adipose tissue compartment, as ovarian excision leads to short-term changes in the pattern of interleukin-1beta and interleukin-10 cytokine production that precede body weight gain and are not reverted by estradiol replacement.     

Ghrelin and the Hyposomatotropism of Obesity

Objective: Human obesity is characterized by growth hormone (GH) deficiency, which appears primarily related to a central pattern of obesity and is reverted on weight loss. As yet, the metabolic basis of the GH deficiency remains to be elucidated. The recently discovered endogenous ligand for the GH secretagogue receptor, ghrelin, stimulates GH secretion when administered to rodents or healthy humans. It may thus be hypothesized that low ghrelin levels underlie the hyposomatropism in obesity. Research Methods and Procedures: We have tested this hypothesis in individuals with widely varying body mass and fat distribution and evaluated whether the improved GH concentrations on weight loss are associated with enhanced ghrelin levels. Results: Both plasma GH and ghrelin levels were reciprocally related with body mass index (r = −0.67, p < 0.001). However, whereas 24-hour GH secretion was negatively related to the visceral fat area (r = −0.72, p < 0.01), ghrelin levels showed a positive relationship with the visceral fat area (r = 0.49, p < 0.02). Weight loss resulted in increased GH secretion (median 24-hour GH area under the curve: 1983 vs. 4024 mU/day before and after weight loss, respectively; p < 0.01) but did not affect ghrelin levels. No relationship could be found between GH and ghrelin plasma levels in obese subjects when comparing diurnal concentration profiles. Discussion: We showed that plasma ghrelin and GH levels are both reciprocally related with body mass index, but no causative relationship could be demonstrated between low ghrelin levels and the hyposomatropism in human obesity.     

Age-related alterations in pulsatile luteinizing hormone release: effects of long-term ovariectomy, repeated pregnancies and naloxone

Aging of the female reproductive system may be regulated by changes at the hypothalamic, pituitary, and ovarian levels. Long-term ovariectomy (LT-OVX) and/or multiple pregnancies delay age-related deterioration of several parameters of reproductive potential in rodents. We tested whether long-term suppression of cyclic ovarian hormone release that is normally associated with the 4- to 5-day estrous cycle decelerates age-related decreases in the frequency of luteinizing hormone (LH) pulses to assess whether hormonal milieu influences the rate of aging of the pulse generator. We determined the percentage of rats exhibiting pulsatile LH secretion, mean LH levels, and amplitude and frequency of LH pulses in seven groups of ovariectomized (OVX) rats. Young (3-4 mo), middle-aged (8-10 mo), and old (18-22 mo) virgin rats, ovariectomized 4 wk (4WK-OVX) prior to experimentation, were used to determine the effect of age. The effect of long-term ovarian hormone deprivation was tested by ovariectomizing rats at 2-3 mo of age and using them when they were middle-aged (8-10 months) or old (18-22 mo). The effect of deprivation of cyclic increases in ovarian hormones associated with repeated estrous cycles was tested by using retired breeder (RB) rats that had been ovariectomized 4 wk prior to experimentation. Each rat was implanted with a right atrial cannula and bled the next day at 10-min intervals for 3 h.(ABSTRACT TRUNCATED AT 250 WORDS)     

Masculinization of growth hormone (GH) secretory pattern by dihydrotestosterone is associated with augmentation of hypothalamic somatostatin and GH-releasing hormone mRNA levels in ovariectomized adult rats.

The role of androgen in the sexual dimorphism in hypothalamic growth hormone (GH)-releasing hormone (GHRH) and somatostatin (SS) gene expression was examined in rats. In the first study, the SS and GHRH mRNA levels were measured in both male and female rats at 4, 6, 8, and 10 weeks of age. A significant sex-related difference in the SS and GHRH mRNA levels was observed after 8 weeks of age, when sexual maturation is fully attained. Male rats had higher SS and GHRH mRNA levels than the female rats. In the second study, adult ovariectomized rats received daily injection of dihydrotestosterone (DHT), nonaromatizable testosterone, at a dose of 2 mg/rat for 21 days. The DHT treatment masculinized the GH secretory pattern, which was indistinguishable from that of intact male rats, and simultaneously augmented the SS and GHRH mRNA levels. The DHT treatment of ovariectomized rats after hypophysectomy significantly raised the level of SS mRNA, but not that of GHRH mRNA compared to the control animals. These findings suggest that the activation of the SS gene expression through androgen receptor plays an important role in the maintenance of sexual dimorphism in GH secretion in rats.     

Effects of sex hormone levels on aortic vascular reactivity and variables associated with the metabolic syndrome in sucrose-fed female rats

We studied the effect of varying levels of sex hormones, induced by ovariectomy and administration of testosterone or estradiol, on aortic reactivity in female rats with metabolic syndrome (MS) induced by a sucrose diet. Vasoreactivity of aortic rings, blood pressure, intra-abdominal fat, serum triglycerides, nitrates and nitrites, and TBARS were evaluated. Intact MS and ovariectomized MS had higher BP than intact control (C) and ovariectomized C, respectively; estradiol administration decreased BP in ovariectomized MS but not in ovariectomized C. Triglycerides and fat were both higher in MS. Triglycerides were not modified by surgery or hormone treatment, but ovariectomy increased fat. When ovariectomy was combined with hormones, however, fat was reduced to the level of intact rats. Ovariectomy decreased, but hormones increased, serum nitrates and nitrites. Vasoconstriction was larger in intact MS and ovariectomized MS + testosterone aortas than in intact C and ovariectomized C + testosterone, respectively. Vasodilation was reduced in intact MS and ovariectomized MS + testosterone compared with intact C, ovariectomized C + testosterone, ovariectomized MS, and ovariectomized MS + estradiol. The results suggest endothelial dysfunction in intact MS and ovariectomized MS + testosterone, but protection by ovariectomy + estradiol in MS due to hormones. Indomethacin reduced all contractions, but the effect was greater in estradiol-treated rats. L-NAME increased contractility, more in the ovariectomized C and MS groups and less in the estradiol-treated groups.     

Pituitary gonadotropin-releasing hormone receptor content in rats with polycystic ovaries

A single injection of estradiol valerate (EV) induces, after a lag period of 4-6 wk, a chronic anovulatory polycystic ovarian (PCO) condition in adult rats. This condition is associated with a selective compromise of luteinizing hormone (LH) release and/or synthesis reflected in low basal serum LH concentrations, decreased pituitary content of LH, and decreased gonadotropin-releasing hormone (GnRH)-stimulated LH secretion. The present study was undertaken to determine to what extent the aberrant LH release in rats with PCO could be related to alterations in pituitary content of GnRH receptors. Pituitary GnRH-receptor content was assessed by the evaluation of saturation binding of a GnRH analog, [125I]-D-Ala6-des-Gly10-GnRH, to pituitary membrane preparations. The receptor content of pituitaries from rats with PCO was compared to that obtained from intact animals at estrus and diestrus. Receptor levels in ovariectomized normal rats and rats with PCO were also assessed. The pituitary GnRH receptor content in PCO rats was similar to that observed in normal controls at estrus and was significantly lower than that for rats at diestrus. Although a twofold increase in pituitary GnRH receptor content was observed at 28 days following the castration of control rats, GnRH receptor content in the pituitaries of PCO rats, at 28 days following ovariectomy, remained unchanged. Although, castration-induced elevations in mean serum LH and follicle-stimulating hormone (FSH) concentrations were observed in both the PCO and control animals, the rise in both gonadotropins was significantly attenuated in the PCO-castrates when compared to the ovariectomized controls. Since GnRH is a major factor in the regulation of pituitary GnRH receptor content, these findings suggest that hypothalamic GnRH release is impaired in rats with PCO and that this impairment is independent of any influences from the polycystic ovaries.     

Estrogen receptors and the activity of nitric oxide synthase in the artery of female rats receiving hormone replacement therapy

OBJECTIVE: To observe the expression of estrogen receptor and the activity of NOS in the arteries of female rats receiving estrogen replacement therapy. METHODS: Seventy-two female rats were randomly divided into four groups: group A: sham-ovariectomy; group B: ovariectomy; group C: ovariectomy with estrogen replacement therapy (benzoate estradiol, 5 microg i.m. once in 2 days); group D: ovariectomy with estrogen and progesterone replacement therapy (benzoate estradiol, 5 microg i.m. once in 2 days and progesterone, 1 mg i.m. once in 2 days). The rats were killed after 2 months. The receptor-binding assay was adopted to measure the estrogen receptors in the arteries of the rats, and the activity of NOS in the arteries was assessed by the hemoglobin reductase method. RESULTS: The ER number and NOS activity in the arteries of the ovariectomized group are less than those in sham-ovariectomy group (p<0.05). The ER number and NOS activity in the arteries of groups C and D are larger and higher than those in the ovariectomized group (p<0.05). No significant differences in the ER number and NOS activity were observed between groups C and D. CONCLUSION: The ER number and NOS activity in the rat artery significantly decrease after ovariectomy, while hormone replacement therapy can significantly increase the artery NOS activity and retain the ER number in the artery of the ovariectomized rats to normal level. The result may contribute to explaining the beneficial effect of estrogen in the prevention of coronary artery diseases in postmenopausal women.