共查询到20条相似文献,搜索用时 78 毫秒
1.
Martin R. Clark John M. Marsh William J. LeMaire 《Prostaglandins & other lipid mediators》1976,12(2):209-216
Preovulatory follicles isolated from immature rats, treated with pregnant mare's serum gonadotropin, were incubated and the accumulation of prostaglandin E measured. The addition of luteinizing hormone (5 μg/ml) increased this accumulation, after a lag period of 3 hours. This delay suggested the involvement of macromolecular synthesis in the mechanism of prostaglandin stimulation by luteinizing hormone. When the synthesis of protein was inhibited by the addition of puromycin (100 μM), the luteinizing hormone stimulation of prostaglandin E in these follicles was completely abolished. This inhibition was not seen with an analogue of puromycin, which does not inhibit protein synthesis, puromycin amino-nucleoside. These data suggest that concomitant protein synthesis is required for the luteinizing hormone stimulation of prostaglandin accumulation in rat follicles. 相似文献
2.
Corticosterone alone was not able to stimulate release of luteinizing hormone (LH) from anterior pituitary cells , but corticosterone in combination with luteinizing hormone releasing hormone (LHRH) augmented the release of LH into the culture media. These results may indicate that corticosterone may have the capacity to activate membrane receptors for LHRH in the gonadotrophs. 相似文献
3.
William B. Wehrenberg Nicholas Ling Paul Brazeau Fred Esch Peter Böhlen Andrew Baird Shao Ying Roger Guillemin 《Biochemical and biophysical research communications》1982,109(2):382-387
The synthetic replicate of a 44 amino acid peptide isolated from a human pancreatic tumor which had caused acromegaly possesses high specific activity to release growth hormone (GH) in anesthetized male rats. The GH secretion induced by this peptide is dose-dependent from 50 ng to 1 μg, with plasma GH concentrations increasing more than 10-fold within 5 min of iv administration at the higher doses. Two enzymatic degradation products of the 44 residue peptide were also isolated and consist of the first 37 and 40 amino acids. All three peptides appear to possess similar potency, on a molar basis, , contrary to results. The specificity of these peptides on GH release was shown by their failure to alter plasma concentrations of prolactin (PRL), thyroid-stimulating hormone (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and corticosterone. Based on these results, the three peptides with serve as powerful tools with which to investigate the mechanisms of GH secretion. 相似文献
4.
A De Flora A Morelli F Giuliano 《Biochemical and biophysical research communications》1974,59(1):406-413
A series of peptide analogs of luteinizing hormone releasing hormone (LH-RH), altered at position 6 and 10, was synthesized and evaluated for the ability to induce ovulation in the diestrous rat and for ability to release pituitary luteinizing hormone and follicle stimulating hormone. All the analogs with D-amino acid substitutions at position 6, even those with large bulky side chain, exhibited an amazingly high potency compared with the parent hormone, LH-RH. On the basis of the biological activities, structure-activity relationships in the central part of this molecule were discussed in detail. 相似文献
5.
J. Osterman E.P. Murono T. Lin H.R. Nankin 《Biochemical and biophysical research communications》1983,112(2):496-501
Possible functional relationship between luteinizing hormone-stimulated ornithine decarboxylase and testosterone production was examined in rat testicular interstitial cells . Although luteinizing hormone enhanced both ornithine decarboxylase activity and testosterone production at a similar physiological dose range, we found dissociation in the two responses in terms of their temporal aspect and the way they were affected by an irreversible inhibitor of ornithine decarboxylase, alpha-difluoromethylornithine, and protein synthesis inhibitor cycloheximide. The results suggest that there appears to be no causal coupling between luteinizing hormone-stimulated enzyme activity and testicular steroidogenesis. 相似文献
6.
The site at which opiate agonists and antagonists act to alter secretion of prolactin, growth hormone and luteinizing hormone as well as the pharmacological specificity of the opiate receptors mediating these effects were examined in rats. Injection of β-endorphin but not a 10 fold higher dose of the non opiate peptide β-endorphin, increased release of prolactin and growth hormone in male rats while inhibiting luteinizing hormone release in ovariectomized, estrogen primed female rats. Prior treatment with naltrexone i.p. blocked these responses. Injection of naltrexone into the hypothalamus lowered prolactin release. In rats with a surgically formed hypothalamic island systemic administration of morphine or naltrexone altered prolactin release in the same manner as was observed in intact animals. In contrast no effects of β-endorphin or naltrexone were observed on the spontaneous secretion of prolactin . In addition β-endorphin did not alter the inhibition of prolactin release produced by apomorphine . The ED50 for stimulation of prolactin release following intraventricular administration of β-endorphin or the synthetic enkephalin analog FK 33-824 was the same, approximately 0.1 ng/rat. However FK 33-824 at 0.2 ng/rat was able to produce much greater analgesia and catatonia than β-endorphin. The metabolism and distribution of β-endorphin was examined but did not account for these differential effects. These results indicate that opiate agonists and antagonists can act at the hypothalamic but not the anterior pituitary level to alter release of prolactin, growth hormone and luteinizing hormone. In addition the data suggest that the opiate receptors mediating release of prolactin may have a different pharmacological specificity from those involved with analgesia and catatonia. 相似文献
7.
J A Villarreal W Vale M Brown M Butcher P Brazeau C Rivier R Burgus 《Biochemical and biophysical research communications》1976,70(2):551-558
A protein has been isolated from ovine hypothalamus on the basis of its ability to stimulate release of growth hormone by cultures of dispersed pituitary cells. This protein has been identified as being myelin basic protein. With no similar biological activity , myelin basic protein is thus to be recognized as a potentially interfering substance in any search for the physiological growth hormone releasing factor using assay systems. 相似文献
8.
Johannes D. Veldhuis Patricia A. Klase 《Biochemical and biophysical research communications》1982,104(2):603-610
The divalent-cation ionophores A23187 and ionomycin exert dose-dependent suppressive effects on the stimulatory actions of luteinizing hormone in ovarian cells . Micromolar concentrations of both A23187 and ionomycin can inhibit the production of progesterone and the stimulation of ornithine decarboxylase activity. Inhibitory concentrations of these ionophores deplete total cell content of calcium, and also seem to suppress protein synthesis. 相似文献
9.
The dynamics of gonadotropin releasing hormone (GnRH) induced luteinizing hormone (LH) release was studied by superfusion of cultured pituitary cells. Continuous exposure of the cells to GnRH resulted in desensitization of the gonadotroph responsiveness to further stimulation by the hormone. The refractory state was achieved within 4 hr of hormone introduction (10?7 M) and was accompanied by down-regulation of GnRH receptors (50%) assayed by equilibration with [125I]iodo-[D-Ala6]des-Gly10-GnRH N-ethylamide. The data indicate that GnRH can regulate the number of its own receptors, and that desensitization is accompanied by down-regulation. 相似文献
10.
A method is described which makes use of 4M MgCl2 to dissociate the testicular luteinizing hormone-receptor complex without altering either the binding capacity or binding affinity of the receptor. Using this method, it was demonstrated that incubation at 4° of decapsulated rat testes with various concentrations of luteinizing hormone or with human chorionic gonadotropin resulted in a reduction in binding capacity. This reduction of binding capacity could not be completely accounted for by occupation of receptors by homologous hormone, suggesting that receptors were lost. Thus negative regulation of LH receptors by LH and hCG was observed. The reduction in LH binding capacity was specific for LH and hCG, dose dependent and time related. FSH, prolactin and growth hormone did not exert the same effect. 相似文献
11.
Experiments were undertaken to investigate if changes occur at the level of the anterior pituitary gland to result in selective follicle-stimulating hormone (FSH) release during late proestrus in the cyclic rat. At 1200 h proestrus, prior to the preovulatory luteinizing hormone (LH) surge in serum and the accompanying first phase of FSH release, serum LH and FSH concentrations were low. At 2400 h proestrus, after the LH surge and shortly after the onset of the second or selective phase of FSH release, serum LH was low, serum FSH was elevated about 4-fold, pituitary LH concentration was decreased about one-half and pituitary FSH concentration was not significantly decreased. During a two hour incubation, pituitaries collected at 2400 h released nearly two-thirds less LH and 2.5 times more FSH than did pituitaries collected at 1200 h. Addition of luteinizing hormone releasing hormone (LHRH) to the incubations caused increased pituitary LH and FSH release. However, the LH and FSH increments due to LHRH in the 2400 h pituitaries were not different from those in the 1200 h pituitaries. The results indicate that a change occurs in the rat anterior pituitary gland during the period of the LH surge and first phase of FSH release which results in a selective increase in the basal FSH secretory rate. It is suggested that this change is primarily responsible for the selective increase in serum FSH which occurs during the second phase of FSH release. 相似文献
12.
R.M. Sharpe D.G. Doogan I. Cooper 《Biochemical and biophysical research communications》1982,106(4):1210-1217
Injection of a luteinizing hormone-releasing hormone (LHRH) agonist into 55-day-old male rats which had been hypophysectomized 3 days earlier resulted in a 10- to 30-fold increase in the levels of testosterone in serum and testicular interstitial fluid (IF) in the 4h following injection. The levels achieved were within or above the normal range for intact untreated rats of this age. In similar animals, injection of LHRH agonist also enhanced the serum testosterone response to injected hCG at , but not at later times after injection, and by 24h reduced IF levels of testosterone suggested that LHRH agonist had begun to inhibit stimulation by hCG. , dispersed Leydig cells from untreated hypophysectomized rats showed a 2-fold increase in testosterone responsiveness to LHRH agonist when compared to cells from intact rats, and this change was associated with an 80% increase in the number of Leydig cell LHRH-receptors. 相似文献
13.
We have recently demonstrated that gonadotropin releasing hormone (GnRH) acts directly on ovarian granulosa cells to inhibit the follicle stimulating hormone (FSH)-induced increase in granulosa cell steroidogenesis . A GnRH antagonist, [D-pGlu1, D-Phe2, D-Trp3,6] GnRH (A), which is known to antagonize GnRH-stimulated gonadotropin release by cultured pituitary cells, was tested in the granulosa cell system. GnRH (10?8M) inhibited estrogen and progesterone production by FSH-treated granulosa cells , whereas the antagonist A (10?6M) did not affect FSH stimulation of steroidogenesis. Antagonist A, when added together with GnRH and FSH, blocked the GnRH inhibition of FSH-induced steroidogenesis. Estrogen and progesterone production by granulosa cells was increased by 50% at a molar ratio (IDR50) of ([antagonist]/[GnRH]), respectively. At 10?6M, antagonist A completely prevented the GnRH (10?8M) inhibition. A similar effect of antagonist A was seen in FSH-induced increase of luteinizing hormone (LH) receptor content. FSH treatment for 2 days induced an 8-fold increase in LH receptor content in cultured granulosa cells; concomitant treatment with 10?8M GnRH completely inhibited the FSH effect. Antagonist A (10?6M), by itself, had no effect on the FSH action. However, when added together with FSH and GnRH, antagonist A completely abolished the inhibitory effect of GnRH. These results demonstrate that the direct inhibitory effect of GnRH on granulosa cell function can be prevented by a GnRH antagonist and that the GnRH action at the ovarian level may require stringent stereospecific interactions of these peptides with putative GnRH recognition sites. 相似文献
14.
J Humphries Y P Wan K Folkers C Y Bowers 《Biochemical and biophysical research communications》1977,78(2):506-509
Substitution of cyclopentylcarbonyl-(Cpc) for 1 in the effective and potent antiovulatory inhibitor, [D-Phe2, Pro3, D-Phe6]-LHRH (I) retained the potency. We know of no other inhibitor of the luteinizing hormone releasing hormone (LHRH) with a modification at position 1, which is as potent . This result agrees with the concept of the role of 1, D-Phe2, Pro3, D-Phe6]-LHRH did not inhibit ovulation in rats at the same dosage as did I; this result is under study to circumvent. Des-Gly10-[D-Phe2, Pro3, D-Phe6]-LHRH ethylamide and [Glu1, D-Phe2, Pro3, D-Phe6]-LHRH were significantly less active than I. 相似文献
15.
Leydig cells isolated from adult rat testes bound 125I-labelled luteinizing hormone releasing hormone (LHRH) agonist with high affinity (KA=1.2 × 109M) and specificity. LHRH and the 3–9 and 4–9 fragments of LHRH agonist competed for binding sites with 125I-LHRH agonist but with reduced affinities, whereas fragments of LHRH, and oxytocin and TRH were largely inactive. Somatostatin inhibited binding at high (10?4M) concentrations but was inactive at 10?6M and less. Pretreatment of rats for 7 days with 5 μg/day of LHRH agonist reduced binding of 125I-LHRH agonist to Leydig cells by 25%, whilst inhibition of endogenous LHRH by antibodies for 7 days caused a 40% decrease. 相似文献
16.
Inhibition of the release of growth hormone in vitro by -melanocyte stimulating hormone 总被引:1,自引:0,他引:1
A V Schally A Arimura A J Kastin T Uehara D H Coy E J Coy J Takahara 《Biochemical and biophysical research communications》1973,52(4):1314-1319
A polypeptide isolated from porcine hypothalami was found to inhibit the release of growth hormone (GH) from isolated rat pituitaries. This polypeptide was identified chemically and biologically as α-MSH. Pure natural α-MSH isolated from beef posterior pituitary extracts and synthetic α-MSH also inhibit the release of GH . In addition, other substances not yet identified, present in porcine hypothalamic extracts, also share this property. 相似文献
17.
R Filler K S Morey G Litwack 《Biochemical and biophysical research communications》1974,60(1):431-439
(3H) 3-Methylcholanthrene binds to a macromolecule in addition to the previously reported binding to ligandin in liver cytosol. The properties of this second molecule are identical to those of the glucocorticosteroid receptor (Binder II) through 400 fold purification over the cytosol proteins (elution position from DEAE-Sephadex A-50 columns, molecular weight by gel filtration and pI value by isoelectrofocusing). The carcinogen, probably a metabolite, binds very strongly or covalently to the macromolecule , but non-covalently in the absence of microsomes. Large amounts of unlabeled carcinogen administered do not compete significantly with subsequent (3H) dexamethasone binding to the hormone receptor fraction . Methylcholanthrene and dexamethasone do not compete for binding sites on isolated unlabeled Binder II leading to the conclusion that the glucocorticosteroid receptor and the methylcholanthrene binding protein are distinct entities. 相似文献
18.
J.F. McKelvy P. LeBlanc C. Laudes S. Perrie Y. Grimm-Jorgensen C. Kordon 《Biochemical and biophysical research communications》1976,73(2):507-515
Bacitracin was found to be an effective inhibitor of the degradation of both thyrotropin releasing factor1 (TRF) and luteinizing hormone releasing factor (LRF) by guinea pig hypothalamic and whole brain homegenates and rat hypothalamic homogenates and subcellular fractions. Bacitracin was effective in inhibiting the degradation of TRF and LRF, as determined by radioimmunoassay, where it exhibited no interference with the assays. Kinetic studies of the degradation of exogenous synthetic [3H]-TRF demonstrated non-competitive inhibition by bacitracin with Ki = 1.9 × 10?5 M, while studies on the degradation of [3H] LRF indicated competitive inhibition with Ki = 1.7 × 10?5 M. Electrophoretic and amino acid analysis revealed that bacitracin itself was not degraded during the course of the incubation. 相似文献
19.
Yvonne Grimm-Jørgensen 《Life sciences》1980,26(15):1211-1216
The effect and metabolic fate of thyrotropin releasing hormone on the cAMP content of incubated ganglia from the pond snail was studied. It was found that TRH caused an increase in the cAMP content of parietal ganglia, a decrease in the cAMP content of cerebral ganglia and no change in the other circumesophageal ganglia. incubated ganglia did not accumulate or degrade significant amounts of 3H-TRH. 相似文献
20.
M Lippman 《Life sciences》1976,18(2):143-152
Steroid hormones induce responses in target tissues by a mechanism involving the specific initial interaction of hormone with cytoplasmic receptor molecules. These receptors, usually localized in target tissues have high binding affinities and limited binding specificities for biologically active steroids. Examination of human leukemic lymphoblasts has revealed these receptors in some tumor samples. Their presence is well correlated with hormone responsiveness of the tumor . Similar studies on human breast cancer tumor homogenates has indicated that about of primary tumors contain estrogen receptor. The absence of receptor predicts a lack of response to hormone therapy almost invariably, while the presence of receptor increases but does not assure that the tumor will be hormone responsive. Recently tissue culture systems which mimic the hormone responses observed have been developed which should significantly aid in the clarification of the mechanisms whereby steroid hormones stimulate and inhibit growth in target tissues. 相似文献