用放射免疫测定法研究性类固醇激素和棉酚对大白鼠垂体LH分泌的影响

用兔抗羊 LH 血清和放射性碘标记的羊 LH 建立了大白鼠血清中 LH 的双抗体放射免疫测定法。在这异源的系统中羊 LH 和大鼠 LH 的剂量反应曲线是平行的。当用羊LH_(2-2-1)作参考标准时测量的灵敏度为0.1ng/管。当用大鼠 LH-RP-1作参考标准时测量的灵敏度为10ng/管。大鼠的 FSH 没有交叉反应,所以 FSH 不会干扰血清 LH 的测定。用这个系统我们研究了去卵巢以及去卵巢后给予孕酮和巳烯雌酚以后大鼠血清中LH 水平的变化。结果表明性类固醇激素对大鼠垂体 LH 的分泌具有一个负反馈的调节机制。本文中还研究了棉酚对大鼠 LH 分泌的影响。我们发现成年雄鼠服用棉酚以后血浆 LH 的水平以及垂体对 LRH 的反应均无显著的变化。结果表明新的男性抗生育药物——棉酚似乎不影响垂体的 LH 分泌功能。     

仙灵骨葆对骨质疏松大鼠OPG/RANK/RANKL 表达的影响

目的:观察仙灵骨葆治疗骨质疏松模型大鼠后,对大鼠体内OPG/RANKL/RANK表达的影响。方法:卵巢摘除法建立SD大鼠骨质疏松模型,设立假手术组、对照组(单纯去卵巢组)、雌激素组(给予17β-雌二醇)和治疗组(给予仙灵骨葆)。术后1周开始给药,给药12周后检测各组大鼠股骨骨密度,ELISA法检测血清中OPG/RANKL含量,RT-PCR检测骨组织中OPG/RANK/RAN-KL mRNA表达,免疫组化检测骨组织中RANK的表达。结果:对照组大鼠骨密度显著低于假手术组;治疗组和雌激素组大鼠O-PG表达显著高于对照组,RANK及RANKL的表达显著低于对照组。结论:采用卵巢摘除法成功建立大鼠骨质疏松模型;仙灵骨葆可促进骨质疏松大鼠OPG的表达,并抑制RANK及RANKL的表达,对骨质疏松模型大鼠有治疗作用。     

羊骨胶原肽钙螯合物对去卵巢大鼠肾组织病变的改善作用

目的探究羊骨胶原肽钙螯合物(collagen peptide chelated calcium,CPCC)对雌激素缺乏大鼠肾的保护作用及相关机制。方法摘除大鼠双侧卵巢,CPCC高(CPCC-H)和低(CPCC-L)剂量组的灌胃剂量分别为5 g/(kg·d)和1 g/(kg·d),假手术组和模型组灌胃等体积蒸馏水。8周后测定肾抗氧化指标并观察肾组织形态学变化; qRT-PCR测定JAK/STAT通路相关基因mRNA表达量。结果与假手术组相比,去卵巢模型组大鼠肾TSOD、GSH-Px和T-AOC水平极显著下降、MDA含量极显著增加(P 0.01),肾组织结构紊乱、淋巴细胞浸润;血清中炎性因子IL-2、TNF-α和IFN-γ水平极显著增加(P 0.01),JAK2、STAT1和STAT3基因mRNA的相对表达量极显著增加(P 0.01)。与模型组相比,CPCC剂量组的T-SOD、GSH-Px和T-AOC水平极显著增加,MDA含量极显著下降(P 0.01);肾组织病变明显减轻,淋巴细胞数量减少;血清中各炎性因子水平极显著下降(P 0.01);JAK2、STAT1和STAT3基因mRNA表达量均极显著下降(P 0.01)。结论 CPCC可抑制去卵巢大鼠的氧化应激水平,可能通过JAK/STAT通路改善肾组织病变。     

性腺素:卵泡液中刺激垂体促性腺激素分泌的肽

作者给22天的未成年雌性大鼠注射孕马血清促性腺激素,于25天处死,取卵巢,将卵泡液处理后得到大鼠卵泡液性腺素(gonadocrinin)的粗制剂。将此性腺素制剂加入垂体细胞单层培养以后,培养液中的LH和FSH均增加。而以同样方式处理大鼠肝脏所得到的制剂无此作用。在大鼠间情期第二天,静脉注射该性腺素,血清LH水平的变化与用LRF处理的大鼠相似。这说明,在体及离体条件下,性腺素均能刺激垂体分泌促性腺激素。离体条件下,性腺素仅仅刺激LH和FSH的分泌,对其它几种垂体激素(PRL、GH及TSH)的分泌均无影响。这提示性腺素的作用具有特异性。用放射免疫测定法证明,该性腺素制剂中没有可测出量的FSH、LH、雌激素、孕酮及睾丸酮。     

雷洛昔酚对大鼠垂体的作用

目的 观察雷洛昔酚是否能诱发出催乳素瘤的动物模型以及对PRL水平的影响,以研究雷洛昔酚对大鼠垂体的作用.方法 雌性Wistar大鼠切除卵巢后,分别在皮下埋植含有雷洛昔酚、雌激素和空白硅胶管,术后8周处死大鼠,检测大鼠体重变化、垂体重量变化、血清催乳素(PRL)水平和垂体组织学变化.结果 雷洛昔酚组与阴性对照组大鼠体重无明显统计学差异,与雌激素组大鼠体重具有统计学差异(P＜0.05);雷洛昔酚组与阴性对照组大鼠垂体重相比无明显差异,与雌激素组大鼠垂体重相比具有统计学差异(P＜0.05);雌激素组大鼠血清PRL水平最高,阴性对照组血清PRL水平最低,雷洛昔酚组介于两者之间,分别与雌激素组、对照组相比较差异均具有统计学意义(P＜0.05);雷洛昔酚组与对照组垂体病理为正常细胞形态,雌激素组垂体病理为PRL瘤表现.结论 雷洛昔酚对大鼠垂体有一定的影响,但不能诱发催乳素瘤.     

内皮素促进下丘脑—垂体—卵巢激素的释放

最近发现,内皮素(endothelin,ET)不仅具有强烈的血管活性作用,还可能作为激素调节肽参与性激素的调节。在下丘脑-垂体-卵巢轴的器官和胎盘都有丰富的ETmRNA和ET受体存在。Kanyicska等在培养的雌性大鼠垂体前叶细胞,应用ET-3(10~(-14)～10~(-6)mol/L)明显抑制垂体前叶细胞分泌催乳素(PRL),增加促黄体生成素(LH)、促卵泡素(FSH)和促甲状腺素(TSH)的释放。ET的刺激效     

抗人卵泡刺激素受体多克隆抗体的制备及其对实验大鼠骨质疏松的抑制作用

近年来,卵泡刺激素(follicle-stimulating hormone,FSH)在骨质疏松中的作用得到了证实。卵泡刺激素受体(FSH receptor,FSHR)在成熟的人破骨细胞及破骨细胞前体即单核细胞表面表达,成为阻断FSH作用的潜在靶点。制备了高滴度的兔抗人FSHR多克隆抗体,采用双侧去卵巢手术方法建立SD(Sprague-Dawley)大鼠骨质疏松症动物模型,观察抗FSHR抗体对大鼠实验骨质疏松症的治疗效果。结果显示,卵巢摘除(ovariectomized,OVX)大鼠经抗FSHR多抗和亮丙瑞林(leuprorelin,LE)治疗两周后,与PBS对照组相比,血清FSH和黄体酮(luteinizing hormone,LH)水平显著降低(P0.05),而雌二醇(estrogen,E2)水平有一定升高,但结果不显著(P0.05)。另外,骨组织化学染色显示多抗和LE治疗组大鼠骨小梁数目增加,断裂现象较少。这些结果初步表明,采用抗FSHR抗体对SD大鼠骨质疏松症具有一定的治疗作用。     

转录因子E2F-1与垂体肿瘤转化基因（PTTG）在大鼠PRL瘤中的表达

目的通过检测垂体肿瘤转化基因（PTTG）与腺病毒E2启动子结合因子1（E2F-1）在大鼠催乳素（PRL）瘤中的表达来探讨两者在PRL瘤发生发展过程中的作用。方法 40只大鼠随机分为两组：实验组（E组,n=20）：皮下植入17β-雌二醇的方法诱发大鼠PRL瘤;对照组（C组,n=20）：皮下植入空白硅胶管。雌激素诱导10周后处死大鼠,心脏穿刺取血,4%多聚甲醛体内灌流取出脑垂体,称重,ELISA方法检测两组大鼠血清PRL水平,垂体组织行病理组织学观察,免疫组化SP方法检测两组大鼠垂体组织中PTTG蛋白质、E2F-1蛋白质的表达。结果雌二醇作用10周后,据垂体重量、垂体组织学变化和血清PRL水平证实PRL瘤诱导成功。PRL瘤组中,PTTG蛋白质、E2F-1蛋白质均明显高于对照组,差异具有统计学意义（P〈0.01）;且PTTG蛋白质和E2F-1蛋白质的表达呈明显正相关（γ=0.764,P〈0.01）。结论 PTTG与E2F-1在大鼠PRL瘤中共同过度表达,参与了大鼠PRL瘤的发生发展。     

卵巢中存在免疫活性的促肾上腺皮质激素

阿黑皮素原(POMC)相关肽存在于几种垂体外组织中;如胎盘,肠道,胰腺,睾丸和卵巢。已证明大鼠卵巢中POMC相关肽是由卵巢产生的。然而人们对POMC的一重要产物促肾上腺皮质激素在哺乳动物卵巢中的分布研究较少。作者用免疫组织化学的方法观察ACTH在羊(正常,妊娠和胚胎),牛、猪、猫、大鼠(正     

不同造模方法对大鼠多囊卵巢综合征模型的影响

目的采用不同方法诱导SD清洁级雌性大鼠多囊卵巢综合征(PCOS)动物模型,造模完成后检测大鼠血清相关激素并观察卵巢局部形态学改变,并探讨其意义。方法分别采用来曲唑、硫酸普拉睾酮钠、硫酸普拉睾酮钠联合HCG诱导大鼠PCO模型,RIA法测定血清LH、FSH、E2、P、T、PRL、INS水平,HE染色后光镜下观察卵巢局部形态。结果A组(对照组)和B组(来曲唑组)比较,B组较A组血清FSH浓度升高,血清P浓度降低,差异有统计学意义(P0.05);B组血清T浓度较A组明显升高,差异有显著统计学意义(P0.01)。D组(硫酸普拉睾酮钠组)与C组(对照组)比较,两组间血清性激素及INS差异无显著性(P0.05)。E组(硫酸普拉睾酮钠联合HCG组)与C组比较,E组血清T浓度、LH/FSH比值较C组升高,差异有统计学意义(P0.05)。E组与D组比较,血清P、T浓度升高,差异有统计学意义(P0.05)。A、C两组卵巢局部形态基本正常,可见发育成熟的卵泡及优势卵泡,B、D、E三组未见优势卵泡,均可见卵巢多囊样改变。结论使用来曲唑或硫酸普拉睾酮钠联合HCG诱导大鼠PCOS模型,无论在影响血清性激素还是卵巢局部形态学改变方面与临床表现很接近,符合动物PCOS造模要求。     

Postnatal ovary is necessary for the maturation of estradiol-induced luteinizing hormone and prolactin surges in female rats

The role of postnatal ovary in the maturation of estradiol (E2)-induced luteinizing hormone (LH) and prolactin (PRL) surges was examined in female rats of Wistar-Imamichi strain. Animals were bilaterally ovariectomized at 24 h after birth, 1 week (w), 2 w, 3 w, 4 w or 6 w of age. At about 10 w of age, every group was primed with estradiol benzoate (E2B) for two days, and on the third day was decapitated at either 0900 h or 1900 h. Anterior pituitary (AP) LH and PRL content was determined in every group of no E2B treatment. Surge-like secretions of LH and PRL were observed at 1900 h, only in rats ovariectomized on or after 4 w of age. AP LH and PRL content was the higher, as ovariectomy was delayed. These results indicate that postnatal ovary is necessary for the maturation of E2-induced LH and PRL surges. Such an effect of ovary is mediated at least by its stimulation of AP LH and PRL content.     

The melanocortin 4 receptor mediates leptin stimulation of luteinizing hormone and prolactin surges in steroid-primed ovariectomized rats

We have previously reported that leptin, the product of the obese (ob) gene, may play a physiologically relevant role in the generation of estradiol/progesterone-induced luteinizing hormone (LH) and prolactin (PRL) surges in female rats. In the present study, we examined whether the stimulatory effect of leptin on the hormonal surges is mediated through the melanocortin (MC) 4 receptor in the brain, as is leptin's effect on feeding behavior. We also explored whether the MC4 receptor participates in tonic stimulation of steroid-induced LH and PRL surges. Experiments were performed on both normally fed and 3-day starved rats, which were ovariectomized and primed with estradiol and progesterone. At 11:00 h on the day of the experiments, the normally fed rats received an intracerebroventricular administration of artificial cerebrospinal fluid (vehicle), SHU 9119 (a nonselective MC3/MC4 receptor antagonist, 1.0 nmol), or HS014 (a selective MC4 receptor antagonist, 1.0 nmol). The 3-day starved rats were given vehicle, recombinant mouse leptin (0.3 nmol), leptin (0.3 nmol) + SHU9119 (1.0 nmol), or leptin (0.3 nmol) + HS014 (1.0 nmol). From 11:00 to 18:00 h, blood was collected every 30 min to measure LH and PRL. The 3-day starvation completely abolished both LH and PRL surges, but leptin significantly reinstated these hormonal surges. Both SHU9119 and HS014 significantly decreased the magnitude of LH and PRL surges in normally fed rats and also significantly blocked the leptin stimulation of the hormonal surges in starved rats. These results suggest that the MC4 receptor may be the pivotal subtype of MC receptors mediating the leptin stimulation of LH and PRL surges. The data also suggest that endogenous MC(s) may tonically stimulate the hormonal surges in normally fed rats via the MC4 receptor. This is the first report describing a physiological role of a specific MC receptor in regulating the reproductive axis.     

Differential changes in the mechanisms controlling luteinizing hormone and prolactin secretion in middle-aged female rats

Serum luteinizing hormone (LH) and prolactin (PRL) concentrations were measured in young (3-4 month old) and middle-aged (10-12 month old) intact female rats on proestrus, in ovariectomized rats after two estrogen injections (estradiol benzoate; EB, 10 micrograms/100 g body weight, s.c.) or after preoptic stimulation in EB-primed ovariectomized rats. Only animals showing regular 4-day estrous cycles were selected for the experiment. The magnitude of proestrous LH surge was significantly smaller in middle-aged than in young rats. Two BE injections, at noon on Days 0 and 3, in ovariectomized middle-aged rats failed to induce surges in LH secretion on Day 4 whereas the same treatment produced LH surges in ovariectomized young rats. The preoptic electrochemical stimulation (50 microA for 60 sec) produced a prompt rise in serum LH levels in ovariectomized EB-primed young but not in middle aged rats. The preoptic stimulation with a larger current (200 microA) induced LH secretin in middle-aged rats. In none of these situations serum PRL concentrations were different between young and middle-age rats. These results suggest differential aging rates in the preoptic mechanisms governing LH and PRL secretion in the rat. The function of the preoptic ovulatory center in responding to the estrogen positive feedback action and inducing LH secretion may become impaired and independent of the PRL control mechanism, even before the regular estrous cycle terminates.     

Effects of estradiol on the prolactin surges and the feedback mechanisms of gonadotropins in pseudopregnant rats

The influences of estradiol on the prolactin (PRL) surges and on the secretion of gonadotropins (LH and FSH) were investigated in the pseudopregnancy (PSP) of acutely ovariectomized rats. The four following experimental groups were prepared: 1) intact PSP as a control, 2) ovariectomy was performed on day 0 of PSP (OVX), 3) a Silastic tube containing estradiol was implanted for day 1-4 into the OVX rats (OVX-E 1-4), and 4) the Silastic tube was implanted for day 5-8 by the same manner into the OVX rats (OVX-E 5-8). In the OVX group nocturnal (N) PRL surges were observed at 0500 h on days 4, 8 and 12 examined, and increased secretions of LH and FSH were noted. In the OVX-E 1-4 group, the N PRL surge was suppressed on day 4, and the suppressed N PRL surge did not occur on day 8, after the removal of the implanted tubes. Diurnal (D) PRL surges with LH surges were observed at 1700 h on day 4 in these rats. Similarly, more remarkable results were obtained on days 8 and 12 in the OVX-E 5-8 group than in the OVX-E 1-4.(ABSTRACT TRUNCATED AT 250 WORDS)     

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。     

Loss of luteinizing hormone surges induced by chronic estradiol is associated with decreased activation of gonadotropin-releasing hormone neurons

Chronic exposure of young ovariectomized rats to elevated circulating estradiol causes loss of steroid-induced LH surges. Such LH surges are associated with cFos-induced activation of GnRH neurons; therefore, we hypothesized that chronic estradiol treatment abolishes LH surges by decreasing activation of GnRH neurons. Regularly cycling rats were ovariectomized and immediately received an estradiol implant or remained untreated. Three days or 2 or 4 wk later, the estradiol-treated rats received vehicle or progesterone at 1200 h, and 7 hourly blood samples were collected for RIA of LH. Thereafter, all rats were perfused, and the brains were examined for immunocytochemical localization of cFos and GnRH. The GnRH neurons from untreated ovariectomized rats rarely expressed cFos. As reported, LH surges induced by 3 days of estradiol treatment were associated with a 30% increase in cFos-containing GnRH neurons, and progesterone enhanced both the amplitude of LH surges and the proportion of cFos-immunopositive GnRH neurons. As hypothesized, the abolition of LH surges caused by 2 or more weeks of estradiol was paralleled by a reduction in the percentage of cFos-containing GnRH neurons, and this effect was delayed by progesterone. These results suggest that chronic estradiol abolishes steroid-induced LH surges in part by inactivating GnRH neurons.     

Divergent regulation of gonadotropin subunit mRNA levels by androgens in the female rat.

To examine the effects of gonadal steroids on the pretranslational regulation of the gonadotropin subunits in the female, adult female rats, beginning 7 or 28 days after ovariectomy, received daily injections of testosterone propionate (T), dihydrotestosterone propionate (D), or estradiol benzoate (E) for 7 days. Intact cycling females and ovariectomized rats that received vehicle served as controls. Serum was obtained for LH and FSH levels to assess changes in gonadotropin secretion. Total RNA from individual rats was recovered and analyzed by blot hybridization with specific radiolabeled cDNA probes for the alpha, LH beta, and FSH beta subunits. Autoradiographic bands were quantitated and standardized to mRNA levels in the intact animals. Ovariectomy resulted in a rise in serum gonadotropin levels and all three gonadotropin subunit mRNA levels. Estrogen replacement resulted in suppression of alpha, LH beta, and FSH beta mRNAs whether given at 7 or 28 days after ovariectomy. In contrast, whereas androgen replacement decreased alpha and LH beta mRNAs, D or T did not consistently suppress FSH beta mRNAs. We conclude that chronic estrogen administration to the castrated female rat uniformly suppresses all three gonadotropin subunit mRNA levels. In female rats, as in male rats, chronic androgen administration fails to negatively regulate FSH beta mRNAs.     

Involvement of the neurointermediate lobe of the pituitary gland in the secretion of prolactin and luteinizing hormone in the rat

The relationship between prolactin (PRL) secretion and the neurointermediate lobe (NIL) of the pituitary gland was investigated. Plasma PRL concentrations in rats bearing anterior pituitaries autografted with or without the NIL to the renal capsule were elevated to equal extents at 1 through 6 weeks after surgery (p > 0.10). PRL levels in ovariectomized rats in which the NIL had been removed surgically (NIL-X) or only visualized (NIL-C) were 3–7 ng/ml 4, 7, and 28 days after surgery (p > 0.10); however, they were slightly higher in NIL-X $\text{vs.}$ NIL-C rats 14 days after surgery (p < 0.05). Plasma luteinizing hormone (LH) concentrations in NIL-C rats increased by 36% from 2 to 4 weeks after surgery (p < 0.05); this increase was not detected in NIL-X rats. PRL and LH surges were induced by estradiol implants in ovariectomized NIL-X and NIL-C rats; the profiles of the PRL surges were superimposable, although the magnitude of the LH surge was only 50% that in NIL-C rats (p < 0.05). These results cast doubt on the importance of the NIL in the regulation of PRL secretion either $\text{via}$ secreting hypophysiotropic hormones or $\text{via}$ conducting anterior pituitary hormones directly to the median eminence. However, the NIL may have a physiologically important role in the regulation of LH secretion.     

Interaction between ovarian and adrenal steroids in the regulation of gonadotropin secretion

Recent work from our laboratory suggests that a complex interaction exists between ovarian and adrenal steroids in the regulation of preovulatory gonadotropin secretion. Ovarian estradiol serves to set the neutral trigger for the preovulatory gonadotropin surge, while progesterone from both the adrenal and the ovary serves to (1) initiate, (2) synchronize, (3) potentiate and (4) limit the preovulatory LH surge to a single day. Administration of RU486 or the progesterone synthesis inhibitor, trilostane, on proestrous morning attenuated the preovulatory LH surge. Adrenal progesterone appears to play a role in potentiating the LH surge since RU486 still effectively decreased the LH surge even in animals ovariectomized at 0800 h on proestrus. The administration of ACTH to estrogen-primed ovariectomized (ovx) immature rats caused a LH and FSH surge 6 h later, demonstrating that upon proper stimulation, the adrenal can induce gonadotropin surges. The effect was specific for ACTH, required estrogen priming, and was blocked by adrenalectomy or RU486, but not by ovariectomy. Certain corticosteroids, most notably deoxycorticosterone and triamcinolone acetonide, were found to possess "progestin-like" activity in the induction of LH and FSH surges in estrogen-primed ovx rats. In contrast, corticosterone and dexamethasone caused a preferential release of FSH, but not LH. Progesterone-induced surges of LH and FSH appear to require an intact N-methyl-D-aspartate (NMDA) neurotransmission line, since administration of the NMDA receptor antagonist, MK801, blocked the ability of progesterone to induce LH and FSH surges. Similarly, NMDA neurotransmission appears to be a critical component in the expression of the preovulatory gonadotropin surge since administration of MK801 during the critical period significantly diminished the LH and PRL surge in the cycling adult rat. FSH levels were lowered by MK801 treatment, but the effect was not statistically significant. The progesterone-induced gonadotropin surge appears to also involve mediation through NPY and catecholamine systems. Immediately preceding the onset of the LH and FSH surge in progesterone-treated estrogen-primed ovx. rats, there was a significant elevation of MBH and POA GnRH and NPY levels, which was followed by a significant fall at the onset of the LH surge. The effect of progesterone on inducing LH and FSH surges also appears to involve alpha 1 and alpha 2 adrenergic neuron activation since prazosin and yohimbine (alpha 1 and 2 blockers, respectively) but not propranolol (a beta-blocker) abolished the ability of progesterone to induce LH and FSH surges. Progesterone also caused a dose-dependent decrease in occupied nuclear estradiol receptors in the pituitary.(ABSTRACT TRUNCATED AT 400 WORDS)     

Estrogen modulates the action of nitric oxide in the medial preoptic area on luteinizing hormone and prolactin secretion

Several substances work as neuromediators of the estrogen direct and indirect (through glial cells or interneurons) action on luteinizing hormone- releasing hormone (LH-RH) neurons in medial basal hypothalamus and medial preoptic area (MPOA).Angiotensin II (AII) in the MPOA stimulates the LH and it inhibits PRL secretion in some situations. On the other hand, the effect of excitatory amino acids on LH and PRL surges during proestrus as well LH surge induced by steroids depend on nitric oxide (NO). In the present study we investigated the participation of MPOA endogenous NO on gonadotropin and PRL secretion mediated by estrogen and AII. Plasma LH, FSH and PRL was determinated in estrogen primed and unprimed ovariectomized Wistar rats that received microinjection of AII or saline into the MPOA, associated or not with a previous microinjection of an inhibitor for NOS. Our results show the following: 1 - there was no change in plasma FSH in estrogen- primed or unprimed ovarictomized related with microinjections of AII or NO antagonist in the MPOA; 2- the increase in LH secretion after ovariectomy depends on, at least in part, NO activity in the MPOA; 3- estrogen may have an indirect negative feedback action on LH-RH neurons in the MPOA through NO; 4- the stimulatory action of AII in the MPOA on LH secretion in ovariectomized rats treated with estrogen depends on NO; 5 - NO in the MPOA stimulates or inhibits PRL secretion depending on the absence or presence of estrogen, respectively; 6- the inhibitory action of AII into the MPOA on PRL secretion does not seem to depend on NO.