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1.
2.
1. The rat hypothalamus (containing the supra-optic nuclei, paraventricular nuclei, median eminence and proximal pituitary stalk) has been incubated in vitro and shown to be capable of releasing the neurohypophysial hormones, oxytocin and arginine vasopressin, at a steady basal rate about one twentieth that of the rat neural lobe superfused in vitro. 2. The hypothalamus and neural lobe in vitro released both hormones in a similar arginine vasopressin/oxytocin ratio of about 1-2:1. However, when release was expressed relative to tissue hormone content, the hypothalamus was shown to release about three times as much arginine vasopressin and six times as much oxytocin as the neural lobe. 3. Dopamine in a concentration range of 10(-3)-10(-9)M caused graded increases in hormone release from the hypothalamus in vitro to a maximum fivefold increase over preceding basal levels. The demonstration that apomorphine also stimulated hormone release whereas noradrenaline was relatively ineffective suggested that a specific dopamine receptor was involved. A separate cholinergic component in the release process was indicated by the finding that acetylcholine stimulated release to a maximum fivefold increase in concentrations of 10(-3)-10(-9)M. 4. The fact that the isolated hypothalamus can be stimulated by dopamine and acetylcholine to release increased amount of oxytocin and arginine vasopressin raises the question of the origin and fate of the hormones released in this way. The possibility that they could be released into the hypophysial portal circulation from median eminence to affect the anterior lobe of the pituitary is discussed. 5. In similar doses, both dopamine and noradrenaline injected into the lateral cerebral ventricles of the brain of the anaesthetized, hydrated, lactating rat caused the release of arginine vasopressin and oxytocin. Apomorphine release both hormones but at a higher dose level and to less effect than the catecholamines. 6. The hormone release induced in vivo by dopamine could be prevented by the prior administration of haloperidol or phentolamine and these antagonists were equally effective in blocking the hormone release due to noradrenaline. The involvement of a specific dopamine receptor was more clearly implicated by the use of pimozide which completely inhibited the hormone release due to dopamine and apomorphine but not that due to noradrenaline. 7. It is suggested that the release of neurohypophysial hormones can be stimulated via a dopaminergic nervous pathway in addition to a cholinergic one. The possibility that the osmoreceptor mechanism for the release of antidiuretic hormone from the neural lobe of the pituitary may involve such a dopaminergic pathway is discussed.  相似文献   

3.
Estradiol stimulation of pituitary cAMP production and cAMP binding   总被引:1,自引:0,他引:1  
The role of 17 beta-estradiol (E2) in the modulation of N6,O2'-dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP)-induced hormone release was examined in pituitary monolayer cultures prepared from intact and ovariectomized female rats. Incubations with 5 mM DBcAMP for 4 h significantly (P less than 0.05) stimulated both luteinizing hormone (LH) and prolactin (PRL) release in pituitary cultures prepared from rats at diestrus and from cycling rats at random stages of the estrous cycle. However, DBcAMP failed to stimulate the LH or PRL release in cultures prepared from ovariectomized rats in which the basal LH and PRL release was approximately three-fold and one-tenth of that in cycling rats, respectively. Pretreatment with 1 nM E2 augmented or restored the DBcAMP-induced LH release but not the DBcAMP-induced PRL release in cultures prepared from cycling or ovariectomized rats, respectively. Furthermore, E2 treatment alone of cultures prepared from cycling rats significantly increased intracellular cAMP concentrations and cAMP-binding activities by at least twofold over that of the non-E2-treated controls. The E2-induced rise in cellular cAMP concentration preceded the E2-induced rise in cAMP binding. These results indicate that the priming effect of E2 on pituitary LH responsiveness to DBcAMP is associated with increased cAMP production and cAMP binding.  相似文献   

4.
The effect of ageing and/or melatonin (MEL) on in vitro gonadotropins, luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) release and tissue content from pituitary and median eminence (ME) were investigated. Gonadotropins and PRL basal release (I-1) from hemipituitaries of young cyclic-rats was decreased by MEL to levels shown in old acyclic rats. Pituitary tissue content of LH and PRL were not affected by ageing or MEL treatment. However, pituitary FSH tissue content was decreased by ageing and MEL, suggesting a different regulatory mechanism. MEL inhibitory influence on pituitary hormones is mainly exerted on the secretory process. This effect is only exerted in young rats. ME LH and PRL release and content were significantly lower than in pituitary. However, FSH release and content in ME showed values similar to those found in the pituitary. This study confirms that the functional capacities of pituitary gland and ME are maintained during reproductive senescence.  相似文献   

5.
The stabilization of low luteinizing hormone (LH) concentrationsduring the period of the ovarian cycle preceding the mid-cycleLH surge seems to be of importance for embryo viability andsurvival. Several studies have stressed the importance of thetimely excess of threshold levels of LH for optimal oocyte quality:LH already initiates the resumption of meiosis when a relativelylow threshold level is reached, whereas a further outburst ofLH release is necessary to reach the threshold level to induceovulation. Hence, the mechanism of LH release should have theability, on the one hand, to limit the LH secretion rate, andon the other, to allow an increased secretion rate, as duringthe LH surge. The functional antagonistic coupling of gonadotrophin-releasinghormone (GnRH) and the ovarian protein gonadotrophin surge-inhibitingfactor or -attenuating factor (GnSIF/AF) provides such a modeof action for the control of LH concentration during the ovariancycle. One of the important regulatory steps in this processis the de-novo synthesis of the so far unidentified pituitaryproteins induced by GnRH. The induction of these proteins isa prerequisite for the increase in the rate of LH release. Becausetheir synthesis is a time-consuming process, the effect becomesvisible in the typical biphasic pituitary LH responses to thepulsatile or continuous administration of GnRH: initially low,with an increase after some time. This phenomenon is also knownas the GnRH self-priming action. It is assumed that the synthesisof these self-priming-associated proteins is necessary to eliminatethe inhibitory effect of GnSIF/AF. GnSIF/AF eliminates the effectof self-priming by neutralizing the biological activity of thepituitary proteins, which are responsible for the increasedrate of LH release. Thus, the pituitary gland is kept in a GnRH-hyporesponsivestate. The major advantage of such a slow protein synthesisdependentregulatory mechanism is that it prevents sudden increases inthe LH secretion rate in response to GnRH. Thus it stabilizeslow LH concentrations to prevent the premature reinitiationof meiosis. However, the enhanced secretion of GnRH and/or thesuppressed release or action of GnSIF/AF may finally lead tothe restoration of the intrinsic LH responsiveness of the gonadotrophsat the start of the mid-cycle LH surge. The antagonistic interactionbetween GnRH and GnSIF/AF, and its implication in the controlof LH release under physiological and pathological conditions,are discussed.  相似文献   

6.
The physiological role of follicle stimulating hormone (FSH)in the regulation of the release of the putative ovarian factorgonadotrophin surge-inhibiting or -attenuating factor (GnSIF/AF)was investigated. Blood FSH concentrations were immunoneutralizedin female rats during different days of the ovarian cycle. FSHantiserum was injected in different protocols to neutralizethe FSH surge(s) and/or basal FSH concentrations. All animalswere killed on the morning of the day of pro-oestrus of thecontrol rats. Hemi-pituitaries were incubated and gonadotrophin-releasinghormone (GnRH) stimulated and basal luteinizing hormone (LH)and FSH releases and pituitary contents were measured. The biologicaleffectiveness of the FSH antiserum was established by monitoringthe histology of vaginal smears and inhibin concentrations intrunk-blood. The predominance of small leukocytes in the smears(low oestradiol bioactivity) and the decreased (bioactive) inhibinsecretion imply that anti-FSH neutralizes FSH bioactivity. Simultaneously,the results showed that all anti-FSH injections did not affectthe biphasic LH response to GnRH in-vitro, which shows an unalteredpresence of GnSIF/AF bioactivity in the blood circulation. Theresults suggest that under physiological conditions GnSIF/AFbioactivity, which keeps the LH responsiveness of the pituitarygland suppressed to the action of GnRH, is not supported byinhibin and not controlled by FSH.  相似文献   

7.
Summary Anterior pituitary function was investigated in ten healthy subjects by administering a combination of 200 µg thyrotropin releasing hormone (TRH), 100 µg gonadotropin releasing hormone (GnRH), 100 µg growth hormone releasing factor (GRF1–44), and 100 µg human corticotropin releasing factor (CRF). The same test protocol was performed in all subjects after pretreatment with 0.25 mg terguride. Five subjects were tested only with TRH and GnRH, five only with CRF, and six only with GRF. There was a prompt increase in all hormones after the administration of the four releasing hormones (RH). Pretreatment with terguride lowered the prolactin (PRL) increase (p<0.01) as well as the thyrotropin (TSH) peak (p<0.05) compared with the test without dopamine agonist pretreatment. The PRL levels after combined RH administration were significantly higher than after TRH and GnRH alone. Although four of the five subjects had higher TSH levels after combined RH administration than after TRH and GnRH alone, the difference was not significant. Other hormones were not significantly influenced by the combined RH administration or dopamine agonist pretreatment. Despite the fact that the interaction of the different releasing hormones and dopamine agonists influences the pituitary hormone response, combined RH administration seems to be a useful test for evaluating pituitary function also in patients receiving dopamine agonist therapy.Abbreviations ACTH Adrenocorticotropic hormone - CRF Human corticotropin releasing factor - DA Dopamine - FSH Follicle-stimulating hormone - GH Human growth hormone - GnRH Gonadotropin releasing hormone - GRF; GRF1–44 Growth hormone releasing factor - LH Luteinizing hormone - PRL Prolactin - RH Releasing hormone (s) - RIA Radioimmunoassay - SE Standard error - TRH Thyrotropin releasing hormone - TSH Thyrotropin Supported by Deutsche Forschungsgemeinschaft (We 439/5-1 and Mu 585/2-2).  相似文献   

8.
Effects of 17 beta-estradiol (E2) on adenosine 3',5'-cyclic monophosphate (cAMP) binding and luteinizing hormone (LH) and prolactin (PRL) responses to N6-O-2'-dibutyryl cAMP (DBcAMP) were examined in pituitary monolayer cultures prepared from female rats. Incubation with 8 mM DBcAMP for 4 h significantly (P less than 0.05) increased both LH and PRL release into medium by two- to threefold. E2 pretreatment augmented the DBcAMP-induced LH release but not PRL release to 160% of the non-E2-treated controls. However, the cellular and total accumulation of both LH and PRL were significantly increased in cultures pretreated with E2. The effect of E2 was time dependent, and the maximal effect was observed after 3 days of treatment. Furthermore, E2 treatment significantly increased cAMP-binding activities to 254% of the non-E2-treated controls. The time course of the E2 effect on cAMP-binding activities closely resembled the time course of the E2 effect on LH and PRL accumulation as well as the DBcAMP-induced LH release. These results suggest that the priming effect of E2 on pituitary LH and PRL responses to DBcAMP is associated with increased hormone synthesis and cAMP binding stimulated by E2 pretreatment.  相似文献   

9.
The effect of aging and melatonin on in vitro pituitary responsiveness to luteinizing hormone-releasing hormone (LHRH) was studied. Young cyclic (3-months-old) control (cyclic-control, N = 15), and melatonin (MEL) treated for 2 months (150 microg/100 g BW) (cyclic-MEL, N = 15), old acyclic (23-months-old) control (acyclic-control, N = 13), and MEL-treated (acyclic-MEL, N = 18) rats were used. The hormones analyzed were luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL). The results showed a different influence of the reproductive status as well as of melatonin on the basal secretion rate of both gonadotropins, i.e. LH and FSH. Only the basal FSH release was significantly reduced in cyclic-MEL and acyclic-controls compared to cyclic-controls. The hemipitutary FSH content raised to values similar to those observed for FSH secretion and only the cyclic-MEL group showed significantly higher FSH pituitary content than for release. LHRH addition to the incubation medium resulted in increased LH release for both cyclic and acyclic rats, but FSH release was only stimulated in acyclic rats. Melatonin treatment blunted this response in both cases. In addition, melatonin treatment inhibited prolactin release in acyclic-MEL group after LHRH stimulation but not the basal levels. Pituitary LH and prolactin contents, were significantly higher than the pituitary LH and prolactin levels released from all groups studied, and were not affected by reproductive senescence nor by exogenous melatonin. These data indicate that aging influences more the secretory than the biosynthetic processes. Melatonin influences is endocrine status-dependent, being inhibitory when pituitary hormones reach their higher values.  相似文献   

10.
Insufficient suppression of LH (premature elevation) and FSH (prolonged release) give rise to blood concentrations which may cause damaging effects on oocyte viability and too many follicles respectively. During the surge, LH rises from low to high threshold values to initiate processes from initiation of the resumption of oocyte meiosis to the induction of ovulation. In general, it is thought that a dramatic increase in LH concentration is required to attain the high threshold for ovulation. A self-priming mechanism, by which gonadotrophin-releasing hormone (GnRH) enhances the LH (and FSH) responses to its own action, was thought to be responsible. However, normal LH surges in rats consist of <2-7% of the maximal pituitary releasing capacity. The physiological roles of LH and FSH favour a control mechanism that restrains their blood concentrations during most of the cycle. Ovarian proteins, e.g. inhibin and putative gonadotrophin-surge-inhibiting factor/attenuating factor (GnSIF/AF), are involved in this process. We argue that the increased pituitary LH responsiveness during the mid-cycle surge is not the result of a self-priming process that 'dramatically' increases the LH releasing capacity of the pituitary gland. This is probably due to elimination by GnRH of the inhibitory action of the putative ovarian proteins GnSIF/AF.  相似文献   

11.
Lactotroph secretory activity is regulated by hypothalamic stimulating and inhibiting factors as well as peripheral endocrine hormones. In addition to this important control domain, the pituitary gland displays an intrinsic regulatory ability through autocrine and paracrine signals. To evaluate the role of gonadotrophs in the regulation of prolactin (PRL) secretion, a comparative study was performed applying two regulatory agents that operate through different physiological mechanisms: gonadotropin-releasing hormone (GnRH), which releases regulatory factors co-localized in secretory granules of gonadotrophs, stimulating PRL secretion from lactotrophs; and angiotensin II (AII), with direct effects on lactotroph secretion through specific receptors. In these studies performed in regular and purified primary pituitary cell cultures from female rats, the lactotrophs comprised the largest population of cells (about 51%), whereas gonadotrophs represented only a small fraction (3%) of the total pituitary cell count. In regular cell cultures treatments with AII and GnRH showed a similar secretory behavior, increasing PRL output 73% and 63%, respectively. The stimulation with GnRH and AII of cell cultures with purified lactotrophs and gonadotrophs provided comparable results, but the response of lactotrophs was significantly higher (106% and 138%, respectively) than that recorded in regular cell cultures. Simultaneous AII treatment with an antipeptide antagonist to AII receptor (AII-antipep) completely blocked the PRL release induced by AII. The co-incubation of cells with GnRH and AII-antipep suppressed the peak of PRL release caused by GnRH, confirming that AII is a paracrine agent released by gonadotrophs stimulated with GnRH. The different secretory behavior of lactotrophs treated with AII and GnRH in both regular and purified cell cultures is indicative of the degree of functional interactions between different pituitary cell types. The present study supplies morphological and functional information on the cell-to-cell interactions, which plays an important role in the intrinsic regulatory control of PRL secretion.  相似文献   

12.
The effects were studied of follicle stimulating hormone (FSH)-inducedproduction of gonadotrophin surge-inhibiting factor (GnSIF)on three phases of the pituitary responsiveness to gonadotrophinreleasing hormone (GnRH): the unprimed, primed and desensitizedphases. Rats were injected with FSH on two occasions duringthe oestrous cycle. Spontaneous luteinizing hormone (LH) surgeswere measured as well as GnRH-induced LH surges on the day ofpro-oestrus during infusions with 100–4000 pmol GnRH/rat/10h, in phenobarbital blocked rats. The spontaneous LH surgeswere attenuated or completely inhibited by the FSH treatment.FSH suppresses and prolongs the unprimed LH response and delaysGnRH self-priming, especially during infusions with low concentrationsof GnRH. This treatment does not affect the total LH response(area under curve) to the highest concentrations of GnRH andafter ovariectomy. On the other hand, this response is suppressedduring infusions with the lower concentrations of GnRH. Hence,FSH, via GnSIF, delays maximal priming of the LH response toGnRH, whereas the suppression of LH release is a consequenceof the GnRH-induced progressed state of desensitization. Theinconsistent effects of FSH on the mid-cycle LH surges are explainedas a result of the interaction between the relative strengthsof GnRH and GnSIF.  相似文献   

13.
The effect of follicle stimulating hormone (FSH) treatment on the pituitary response to gonadotrophin-releasing hormone (GnRH) was studied in rats in various reproductive conditions. A 3-day treatment of cycling rats with FSH (Metrodin; 10 IU/injection) lowered the spontaneous pre-ovulatory. LH-surge and suppressed the pituitary luteinizing hormone (LH) response to GnRH. FSH also suppressed the LH response of pseudopregnant (PSP) rats on day 8 of pseudopregnancy, but not that of day-8 PSP rats which had been ovariectomized on day 4 (OVX-PSP rats). GnRH induced self priming in cycling, PSP and OVX-PSP rats. Oestradiol strongly augmented the pituitary LH-response to GnRH injection in PSP and OVX-PSP rats, but not in cycling rats; probably because in these latter animals the LH response to GnRH was already augmented by endogenous oestradiol. FSH suppressed the LH response to GnRH in oestradiol-treated PSP and cycling rats; in these latter rats the suppression of the LH response was as strong as that in cycling rats not treated with oestradiol. FSH did not suppress the LH response of oestradiol-treated OVX-PSP rats. The effect of FSH was not associated with changes in plasma oestradiol and progesterone concentrations. Analysis of the data revealed that FSH specifically suppressed the augmentative effect of oestradiol, but did not affect the GnRH-self priming effect. It is concluded that under the influence of FSH, the ovaries produce a factor which suppresses the augmentative effect of oestradiol on the GnRH-induced LH response of the pituitary gland. It is suggested that this effect of FSH underlies the suppression of the spontaneous LH-surges of FSH-treated cycling rats. As the present putative 'oestrogen-antagonizing factor' did not suppress the GnRH-self priming effect, it is suggested that this factor is not identical to gonadotrophin surge inhibiting factor.  相似文献   

14.
Insulin-like growth factors are involved in the regulation of gonadotropin secretion. Insulin-like growth factor I (IGF-I) has an augmenting effect on gonodotropin-releasing hormone (GnRH)-induced luteinizing hormone (LH) release from female rat gonadotrophs that is facilitated by estradiol. To identify the underlying mechanisms, we investigated whether IGF-I influences total LH pool and the production of intracellular inositol phosphate. In another series of experiments we tested whether IGF-II and estradiol affect LH release of gonadotrophs. Pituitary cells were incubated with 100 pM IGF-I and/or 100 pM estradiol for 24 h. They were stimulated, partially in the presence of Wortmannin, an inhibitor of phosphoinositide 3-kinase, with 330 pM GnRH for 3 h. Subsequently, total LH pool (released and remaining hormone content in lysed cells) in cultures was measured. Intracellular inositol trisphosphate of alphaT3-1 cells, a gonadotrope cell line, treated with estradiol and IGF-I as described before and stimulated with 100 nM GnRH for 15 min was analyzed by ion exchange chromatography. To determine the interaction of IGF-II and estradiol on GnRH-stimulated LH secretion, cells were treated with increasing concentrations of IGF-II (0.05 pM-10 nM) and 100 pM estradiol. IGF-I significantly increased the accumulation of inositol trisphosphate in basal and GnRH-stimulated cells. IGF-I, estradiol, or their combinations did not change total LH pool, although they enhanced LH secretion. Wortmannin abolished the positive effects of IGF-I and estradiol on LH secretion. IGF-II alone increased basal, but not GnRH-induced LH secretion at low concentrations (0.05 pM). Additional estradiol treatment further increased basal, but not GnRH-induced LH secretion. In conclusion, our results suggest that increased LH secretion from female anterior pituitary cells after IGF treatment is due to the amplification of early signal transduction steps rather than changes in LH pool. The inositol trisphosphate signaling pathway is involved in the regulation of LH secretion from gonadotrophs treated with IGF-I. It is not likely that IGF-II plays an important role in the regulation of gonadotropin secretion.  相似文献   

15.
Pulsatile luteinizing hormone (LH) release is thought to becontrolled by the functional antagonism between gonadotrophin-releasing hormone (GnRH) and the putative ovarian factor gonadotrophinsurge-inhibiting/attenuating factor (GnSIF/AF). Our experimentswere designed to titrate the input of endogenous basal and folliclestimulating hormone (FSH)-stimulated GnSIF/AF in this system.The effects were studied of five consecutive pulses of GnRHadministration (10-250 pmol/pulse/kg rat), 1 h apart, on theself-priming effect in pro-oestrus phenobarbital-blocked ratsinjected with FSH or saline. In response to the two high pulsesof GnRH, a clear GnRH self-priming was demonstrated. However,pulses of 25 pmol GnRH induced only a minor self-priming effectand the LH blood concentrations were within the physiologicalrange. Pulses of 10 pmol GnRH had no effect. FSH suppressedthe unprimed LH response and delayed GnRH self-priming by {smalltilde}1 h. Increasing the GnRH pulse frequency of the 25 pmolGnRH pulses from one to three per hour induced pre-ovulatory-likeLH surges. The effect was facilitated by ovariectomy to eliminateGnSIF/AF. Thus, the results are consistent with relative inputsof GnRH and GnSIF/AF being responsible for the changes in LHconcentration during the ovarian cycle, including the generationof the mid-cycle LH surge.  相似文献   

16.
The aim of this study was to find the minimal effective daily s.c. dose of the gonadotrophin-releasing hormone (GnRH) agonist, triptorelin acetate, that suppresses the GnRH-induced release of luteinizing hormone (LH) at time of human chorionic gonadotrophin (HCG) injection and thereby prevents spontaneous LH surges during in-vitro fertilization (IVF) stimulation cycles. Therefore, a double-blind, prospective and randomized titration study was performed. A total of 48 IVF patients were divided into four groups of 12 patients. Each group received a different dose of triptorelin acetate, namely 5, 15, 50 or 100 microg s.c. daily. Standard ovarian stimulation was carried out using urinary follicle stimulating hormone (FSH) preparations. A 500 microg GnRH test was performed 90 min before the HCG injection in order to measure the degree of pituitary desensitization. Spontaneous LH surges were not detected in any of the groups, although three patients in the 5 microg group had ovulated at the time of ovum retrieval. The pituitary LH response to the GnRH test at time of HCG, expressed as area under the curve (AUC), appeared to be dose-dependent. Thus, a daily s.c. dose of 100 microg triptorelin acetate appears to be too high, since adequate desensitization of the pituitary (i.e. no spontaneous LH surge) can be achieved with doses as low as 15 and 50 microg.   相似文献   

17.
The determination of the efficacy of gonadotrophin-releasing hormone (GnRH) antagonists in blocking the luteinizing hormone (LH) surge and luteal function is important for our understanding of the control of the menstrual cycle and for clinical application. GnRH antagonists have failed to block the LH surge reliably in the non-human primate. The aim of the study was to utilize high dose GnRH antagonist treatment administered during the late follicular phase of the menstrual cycle to block the pre-ovulatory LH surge. It was postulated that the LH surge would be prevented in all animals, but if this failed subsequent luteal function would be blocked by continued suppression of LH, since the early corpus luteum is susceptible to inhibition by GnRH antagonist treatment. A group of 16 adult female stumptailed macaques (Macaca arctoides) with regular menstrual cycles were selected. The GnRH antagonist [N-Ac-D-Nal(2)1,D-pCl-Phe2,D-Pal(3)3,D-(Hci)6, Lys(iPr)8,D- Ala10]GnRH (Antarelix) (concentration 10 mg/ml) was administered as three daily s.c. injections, at a dose of 1 mg/kg on days 11, 12 and 13 of the follicular phase of the menstrual cycle. Of nine macaques in which it was judged that the treatment was commenced within 1 day of the expected LH surge (serum oestradiol >400 pmol/l), six demonstrated a decline in serum oestradiol concentrations, a total block of the LH/follicle stimulating hormone (FSH) surge and inhibition of ovulation as judged by an absence of a rise in progesterone concentrations. In the three other animals in this category, a partial LH surge occurred, but this failed to result in a functional corpus luteum. In a further three animals treatment was initiated on the day of the LH surge, and again there was absence of a subsequently functional corpus luteum. These results show that GnRH is involved at the time of the mid-cycle LH/FSH surge in the non-human primate. Initiation of high dose GnRH antagonist treatment during the periovulatory period abolishes luteal function irrespective of its effects upon the LH surge because of its long-term action and resultant withdrawal of luteal support.   相似文献   

18.
GnRH is capable of inducing an increase in cyclic AMP (AMPc) production in the anterior pituitary gland. However, this intracellular messenger is not involved in the mechanisms leading to acute release of gonadotropins. Using anterior pituitary cells in culture, we recently found that AMPc, like GnRH, stimulated the expression of genes encoding for LH and consequently increased the synthesis of LH subunits. To reevaluate the role of AMPc in the secretion of pituitary gonadotropins, we first studied the effects of 8-Br-AMPc, a permeant AMPc analog, on LH release during a 48-hour period. Direct activation of protein kinases A by 8-Br-AMPc substantially stimulated LH release, to values as high as those seen with GnRH under the optimal conditions used in this experiment. However, kinetics were different, with GnRH inducing a rapid rise in LH and 8-Br-AMPc causing a gradual increase after a five-hour lag. We also studied the effects of 8-Br-AMPc on the release of neosynthesized subunits. Pituitary cells were incubated with 35S-Met, and labeled alpha and LH beta polypeptides were recovered in parallel from the cells and medium. We observed that 8-Br-AMPc stimulated not only LH synthesis but also release of newly synthesized LH subunits, in this respect 8-Br-AMPc was more effective than GnRH. After five hours incubation with 1.5 mM 8-Br-AMPc, 95% of the alpha subunit and 40% of the LH beta subunit that had been newly synthesized were released into the medium, whereas the corresponding figures with exposure to 10 nM GnRH were 80% and 15% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

19.
Prolactin (PRL) is under short-loop inhibitory control via the hypothalamus. However, earlier studies evaluated the effects on PRL secretion of PRL levels elevated for periods of days. In this study we evaluated the acute effects of intraventricular and systemic injection of PRL on the release of a variety of pituitary hormones. Ovariectomized (OVX) rats, bearing implanted third ventricular and jugular cannulas were used. Blood was withdrawn in unanesthetized, freely moving animals before and after intraventricular injection of 0.9% NaCl or 1 or 3 micrograms of bovine (b) or ovine (o) PRL. Prolactin was also administered intravenously in doses of 3 or 6 micrograms. No effect on plasma levels of any of the pituitary hormones occurred after intraventricular or systemic injection of saline. Intraventricular injection of both doses of bPRL or oPRL significantly lowered plasma PRL within 15-30 min. In animals with elevated initial PRL values because of stress or estradiol (E) priming, greater lowering of PRL occurred. Inconsistent reductions in plasma PRL occurred after intravenous injection of oPRL but not bPRL, which elevated PRL values via cross-reaction in the immunoassay. In contrast, only small and inconsistent declines in luteinizing hormone (LH) were seen after intraventricular injection of PRL in either OVX or OVX E-primed rats. Plasma follicle-stimulating hormone (FSH) and growth hormone (GH) were not affected by PRL in any of the experiments; however, a significant lowering of thyrotropin (TSH) occurred in OVX or OVX E-primed rats within 30 min after intravenous injection of 3 micrograms of oPRL, but no change occurred after intravenous PRL. The data indicate that PRL can acutely inhibit PRL and TSH release via a hypothalamic action, whereas release of LH is only slightly inhibited and that of FSH and GH is unaltered.  相似文献   

20.
Lipoxygenase metabolites of arachidonic acid were shown to stimulategonadotrophin release dose-dependently in rat pituitary cells.The secretory activity of the arachidonate metabolite leukotrieneC4 (LTC4 was biphasic and 10-fold more potent than that of thephysiological stimulus gonadotrophin-releasing hormone (GnRH).In pre-labelled, superfused pituitary cells, GnRH dose-dependentlyenhanced the release of [3H]arachidonic acid, which occurredsimultaneously with the secretion of luteinizing hormone (LH).When cells were pre-treated with GnRH for 24 h no response toa further stimulus by GnRH (10–7 M) could be observedfor either [3]arachidonate nor LH, demonstrating that also indesensitized cells these two mechanisms react similarly. Inaddition, a GnRH antagonist did not affect the release of arachidonateor LH. These results suggest that arachidonic acid may be involvedin the mechanism of GnRH action on gonadotrophins via its lipoxygenasemetabolites and LTC4 could act as a very potent intracellularstimulus of LH secretion.  相似文献   

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