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1.
The frequency of spontaneous in vitro contractions of seminiferous tubules of the rat appeared to be increased in a dose-dependent manner by prostaglandin F1α. PGF1α treatment increased the tonus of the smooth muscle cells in the wall of the tubules as indicated by a reduction in the diameter of the tubules. When the tubules were rinsed successively with fresh Tyrode's solution, the contractile frequency was diminished. Returning the original bathing medium to the tubules restored their contractile frequency, as did treatment of the rinsed tubules with PGF1α (10−7 M). Pre-injecting the rats with indomethacin tended to reduce the contractile frequency of the extirpated tubules. Treating the tubules with a solution of indomethacin for 90 min. in vitro was more effective than pretreatment in vivo in reducing contractile frequency, but a combination of these two procedures produced the greatest inhibition. PGF1α restored the contractile frequency of the indomethacin-treated tubules. Our results indicate that PGs modulate the in vitro contractility of the tubules. 相似文献
2.
The frequency of spontaneous contractions of seminiferous tubules of the rat appeared to be increased in a dose-dependent manner by prostaglandin F1α. PGF1α treatment increased the tonus of the smooth muscle cells in the wall of the tubules as indicated by a reduction in the diameter of the tubules. When the tubules were rinsed successively with fresh Tyrode's solution, the contractile frequency was diminished. Returning the original bathing medium to the tubules restored their contractile frequency, as did treatment of the rinsed tubules with PGF1α (10-7 M). Pre-injecting the rats with indomethacin tended to reduce the contractile frequency of the extirpated tubules. Treating the tubules with a solution of indomethacin for 90 min. was more effective than pretreatment in reducing contractile frequency, but a combination of these two procedures produced the greatest inhibition. PGF1α restored the contractile frequency of the indomethacin-treated tubules. Our results indicate that PGs modulate the contractility of the tubules. 相似文献
3.
The frequency of spontaneous in vitro contractions of seminiferous tubules of the rat appeared to be increased in a dose-dependent manner by prostaglandin F1alpha. PGF1alpha treatment increased the tonus of the smooth muscle cells in the wall of the tubules as indicated by a reduction in the diameter of the tubules. When the tubules were rinsed successively with fresh Tyrode's solution, the contractile frequency was diminished. Returning the original bathing medium to the tubules restored their contractile frequency, as did treatment of the rinsed tubules with PGF1alpha (10(-7) M). Preinjecting ther rats with indomethacin tended to reduce the contractile frequency of the extirpated tubules. Treating the tubules with a solution of indomethacin for 90 min. in vitro was more effective than pretreatment in vivo in reducing contractile frequency, but a combination of these two procedures produced the greatest inhibition. PGF1alpha restored the contractile frequency of the indomethacin-treated tubules. Our results indicate that PGs modulate the in vitro contractility of the tubules. 相似文献
4.
Hiroshi Yamamoto Toshiaki Endo Tamotsu Kiya Taeko Goto Satoru Sagae Eiki Ito Hiroshi Watanabe Ryuichi Kudo 《Prostaglandins & other lipid mediators》1995,50(4)
In rat luteal cells labeled with (3H]oleic acid, PGF2α-stimulated phospholipase D (PLD) activation was investigated. The PLD activity was detected by measuring the accumulation of [3H]phosphatidylethanol (PtdEt) in the presence of ethanol. PGF2α stimulated PtdEt accumulation at concentrations of more than 100 nM in the presence of ethanol. However, PtdEt accumulation did not change in the absence of ethanol. PGF2α (1 μM) increased PtdEt accumulation after 1 min, and the accumulation reached a plateau by 2–3 min. These results indicate that PGF2α activates PLD in rat luteal cells. U-73122, a phospholipase C (PLC) inhibitor, and staurosporine, a protein kinase C (PKC) inhibitor, did not inhibit PGF2α-stimulated [3H]PtdEt accumulation. These results suggest that PGF2α-induced PLD activation is different from PLC-PKC systems. We reported previously that PGF2α stimulated the release of arachidonic acid. The effects of indomethacin, nordihydroguaiaretic acid (NDGA), and 5,8,11,14-eicosatetraynoic acid (ETYA), inhibitors of arachidonic acid metabolism, on PGF2α-stimulated PtdEt accumulation were examined. Pretreatment with indomethacin enhanced PGF2α-induced PtdEt accumulation. In contrast, pretreatment with NDGA and ETYA inhibited PGF2α-induced PtdEt accumulation. It is suggested that PGF2α-stimulated PLD activation is mediated via lipoxygenase products. 相似文献
5.
The present study has been performed to investigate how PGs would participate the hatching process. Effects of indomethacin, an antagonist to PGs biosynthesis, on the hatching of mouse blastocysts were examined in vitro. Furthermore, it was studied that prostaglandin E2 (PGE2), prostaglandin F2α (PGF2α) or 6-keto-prostaglandin F1α (6-keto-PGF1α) were added to the culture media with indomethacin. (1) The hatching was inhibited by indomethacin yet the inhibition was reversible. (2) In the groups with indomethacin and PGE2, no improvement was seen in the inhibition of hatching and the inhibition was irreversible. (3) In the groups with indomethacin and PGF2α, inhibition of hatching was improved in comparison with the group with indomethacin. (4) In the groups with indomethacin and 6-keto-PGF1α, no improvement was seen. The above results indicated that PGF2α possibly had an accelerating effect on hatching and a high concentration of PGE2 would exert cytotoxic effect on blastocysts. 相似文献
6.
A.L. Gimeno M. Chaud A. Bonacossa A.M. Franchi M.F. Gimeno 《Prostaglandins & other lipid mediators》1983,26(4):663-676
Dose-response curves for several prostaglandins (PGI2; PGD2; PGF2 and PGE2); BaCl2 or prostaglandin metabolites (15-keto-PGF2α; 13, 14-diOH-15-keto-PGF2α; 6-keto-PGF1α and 6-keto-PGE1 in quiescent (indomethacin-treated) uterine strips from ovariectomized rats, were constructed. All PGs tested as well as BaCl2, triggered at different concentrations, evident phasic contractions. Within the range of concentrations tested the portion of the curves for the metabolites of PGF2α was shifted to the right of that for PGF2α itself; the curve for 6-keto-PGF1α was displaced to the right of the curve for PGI2 and that for 6-keto-PGE1 to the left.It was also demonstrated that the uterine motility elicited by 10−5 M PGF2α and its metabolites was long lasting (more than 3 hours) and so it was the activity evoked by PGI2; 6-keto-PGF1α and BaCl2, but not the contractions following 6-keto-PGE1, which disappeared much earlier. The contractile tension after PGF2α; 15-keto-PGF2α; 13, 14-diOH-15-keto-PGF2α and PGI2, increased as time progressed whilst that evoked by 6-keto-PGF2α or BaCl2 fluctuated during the same period around more constant levels.The surprising sustained and gradually increasing contractile activity after a single dose of an unstable prostaglandin such as PGI2, on the isolated rat uterus rendered quiescent by indomethacin, is discussed in terms of an effect associated to its transformation into more stable metabolites (6-keto-PGF1α, or another not tested) or as a consequence of a factor which might protects prostacyclin from inactivation. 相似文献
7.
Shiro Ohki Katsuhiro Imaki Fumio Hirata Toshio Hanyu Nobuhiko Nakazawa 《Prostaglandins & other lipid mediators》1974,6(2)
Radioimmunoassays for measuring prostaglandin F2α (PGF2α) and 5α, 7α-dihydroxy-11-keto tetranorprosta-1,16-dioic acid, PGF2α-main urinary metabolite (PGF2α-MUM), with 125I-tyrosine methylester amide (TMA) of PGF2α and PGF2α-MUM were developed.Antibody to PGF2α was produced in rabbits immunized with conjugates of PGF2α coupled to bovine serum albumine. Antibody to PGF2α-MUM was also produced in rabbits immunized with conjugates of PGF2α-MUM coupled to bovine serum albumin.PGF2α-125I-TMA had an affinity to antiserum to PGF2α. PGF2α-MUM-125I-TMA also responded to antiserum to PGF2α-MUM. 相似文献
8.
Healthy volunteers received 60 μg of [8,10,10-2H3] PGF2α by intravenous infusion both before and during a course of treatment with indomethacin (200 mg/day). Excretion of deuterated 5α, 7α-dihydroxy-11-ketotetranor-prostane-1, 16-dioic acid in urine was quantified by GC-MS using a reverse stable isotope dilution procedure. Indomethacin was found to have no detectable effect on the metabolism of the labelled PGF2α whereas output of the endogenous metabolite was markedly reduced by the effect of the drug on prostaglandin biosynthesis. 相似文献
9.
The effects on the beating behavior of cultured rat heart cells of fourteen prostaglandins of the A, B, D, E, and F series were investigated, together with adrenaline and ouabain, at dose levels of 10−7 and 10−5M. Single heart cell beating activity was monitored photo-electrically and five parameters of beating behavior measured. Only PGF2a markedly increased rate while PGF2B reduced it. Maintenance of a stable rate (rate range) was minimally affected by prostaglandins with PGF2β possibly reducing, and PGF1α and 2-decarboxy E1 possibly increasing, rate range. PGF1α and F2α both statistically reduced the percentage of cells beating while the other prostaglandins had no effect. Most of the prostaglandins either produced no change, or reduced, indices of contractile force (optical density changes with contractions and its first derivative (dOD/dt)). Only the negative chronotropic agent PGF2β positive density effect. In conclusion, except for PGF2α, prostaglandins generally have limited actions on the beating activity of cultured heart cells. 相似文献
10.
Edward E. Wallach M.D. Richard Bronson M.D. Yasuo Hamada M.D. Karen H. Wright B.S. Vernon C. Stevens Ph.D. 《Prostaglandins & other lipid mediators》1975,10(1):129-138
Six mature female rhesus monkeys were treated with HMG-HCG in control cycles at doses adjusted to induce ovulation while avoiding superovulation. Occurrence of ovulation was determined by observation of fresh ovulation points at laparotomy 48 to 120 hours following HCG. In subsequent cycles animals were treated with indomethacin (treatment days 4 through 10) together with the established dose of HMG_HCG. In 8 cycles indomethacin 5 mg/kg was given i.m. once daily; in 9 cycles 10 mg/kg i.m. was administered in 2 divided doses. Following this, PGF2α (3 mg t.i.d. s.c.) was administered for 3 days together with indomethacin 10 mg/kg and HMG-HCG, beginning on the day prior to HCG. Determinations of progesterone were performed by RIA on treatment days 4, 7, 10, and 11. Eleven of the 13 control cycles were ovulatory. With indomethacin 5 mg/kg/day, 5 of 8 cycles were ovulatory but ovulation was delayed in 2 instances. Of 9 cycles using indomethacin 10 mg/kg/day only 1 was ovulatory. When PGF2α was administered in subsequent cycles along with indomethacin (10 mg/kg) and HMG-HCG, ovulation occurred in 13 of 19 cycles. These data suggest that local ovarian PGF2α may be essential in the mechanics of follicle rupture in gonadotropin-treated rhesus monkeys. 相似文献
11.
The mechanism of stimulatory and inhibitory action of PGF2α on ovarian steroidogenesis both under
and
conditions has been studied in the pseudo-pregnant rabbits. Short term incubation of the ovaries with PGF2α (2.82 × 10−5M) resulted in an increased synthesis of progesterone and 20α-OH P. The addition of PGF2α in the medium and further incubation of the ovaries obtained from rabbits that had been constantly infused with PGF2α (0.5 μg/min.) for two hours resulted in increased synthesis of these progestins. The ratio of progesterone to 20α -OH P was also enhanced under these conditions and thus supported the luteotropic action of small doses of PGF2α under short term incubations. However, as the amount of PGF2α infused was increased to 5 μg/min., the addition of PGF2α under
conditions strikingly decreased the production of these progestins. The ratio of progesterone to 20α -OH P was also decreased and thus was indicative of luteolytic action of higher doses of PGF2α. High doses of PGF2α (5.64 × 10−4M) failed to I cause any significant change in the progestin synthesis under short term incubation. These results thus suggest that the luteotropic and luteolytic action of PGF2α in the luteinized rabbit ovary is dose and time dependent. 相似文献
12.
H. Karppanen Anna-Leena Sirn Alice Eskeli-Kaivosoja 《Prostaglandins & other lipid mediators》1979,17(3):385-394
Administration of PGF2α (0.2–6.4 μg) into the lateral cerebral ventricle (i.c.v.) induced dosedependent increases in blood pressure, heart rate and body temperature in urethane-anaesthetised rats, but had no effect on these parameters when the same dose range was administered intravenously. Peripheral pretreatment with sodium meclofenamate (50 mg/kg s.c.) shifted all the dose-response curves for PGF2α (i.c.v.) to the left, but indomethacin (50 mg/kg s.c.) did not significantly affect those changes. Central pretreatment with sodium meclofenamate or indomethacin (1.25 mg per rat i.c.v.) failed to modify significantly the effects of centrally administered PGF2α.The results support previous suggestions that PGF2α may participate in the central control of the cardiovascular and thermoregulatory systems, and also suggest that there may be differences in the sites and/or modes of action between sodium meclofenamate and indomethacin. 相似文献
13.
Ray V. Haning Jr. Leslie Choi Amber J. Kiggens Donna L. Kuzma John W. Summerville 《Prostaglandins & other lipid mediators》1982,23(1):29-40
Explants from term human placentas were maintained in culture with daily changes of medium. Daily output of PGF2α and PGFM1 decreased during the course of the incubation. Addition of 4 μg/ml DHEAS or 67 μg/ml LDL cholesterol had no effect on output of PGF2α or PGFM. Addition of 1.6, 3.2, or 6.4 μg/ml of LHRH to the culture plates had no effect on output of PGFM or PGF2α, but LHRH increased hCG output. Dibutyryl cAMP (1mM, 2mM, and 4mM) increased output of PGF2α, PGFM, and hCG. Aromatase inhibitor decreased hCG output, but it was without effect on output of PGF2α, or PGFM. Significant correlations were demonstrated between progesterone, PGFM, PGF2α, and hCG, suggesting that PGF2α originates in the syncytiotrophoblast cell. The ability of LHRH to stimulate output of hCG but not PGF2α while dbcAMP stimulated both suggests that either PGF2α and hCG arise in different cells or that LHRH does not act through cAMP. 相似文献
14.
In vitro stimulation of prostaglandin synthesis in the rat pancreas by carbamylcholine, caerulein and secretin 总被引:1,自引:0,他引:1
Rat pancreas pieces spontaneously released PGE2 (2.3 ng/100 mg × 45 min) and PGF2α (7.6 ng/100 mg × 45 min). This release corresponds probably to a neo-synthesis since it was abolished by indomethacin. Carbamylcholine (≥ 10 μM), caerulein (≥ 10 nM) and secretin (≥ 10 nM) stimulated the release of PGE2 and PGF2α : the concentrations of stimulators required to increase PGs release were thus much higher than those which trigger enzyme secretion. Atropine specifically inhibited the cholinergic stimulation, whereas indomethacin blocked the stimulatory effects of all secretagogues. Stimulation of PGE2 and PGF2α release was reduced in a Ca++-free medium, abolished by EGTA and mimicked by the ionophore A23187, underscoring the crucial role of Ca++ in the regulation of PGs synthesis by the pancreas. Neither PGE2 nor PGF2α stimulated enzyme secretion in this system and indomethacin did not inhibit the secretory effect of carbamylcholine. Increased synthesis of prostaglandins in response to pancreatic secretagogues does not appear to be involved in the process of enzyme secretion. 相似文献
15.
Dedmer Schaafsma Reinoud Gosens I Sophie T Bos Herman Meurs Johan Zaagsma S Adriaan Nelemans 《Respiratory research》2005,6(1):85
Background
In addition to their proliferative and differentiating effects, several growth factors are capable of inducing a sustained airway smooth muscle (ASM) contraction. These contractile effects were previously found to be dependent on Rho-kinase and have also been associated with the production of eicosanoids. However, the precise mechanisms underlying growth factor-induced contraction are still unknown. In this study we investigated the role of contractile prostaglandins and Rho-kinase in growth factor-induced ASM contraction.Methods
Growth factor-induced contractions of guinea pig open-ring tracheal preparations were studied by isometric tension measurements. The contribution of Rho-kinase, mitogen-activated protein kinase (MAPK) and cyclooxygenase (COX) to these reponses was established, using the inhibitors Y-27632 (1 μM), U-0126 (3 μM) and indomethacin (3 μM), respectively. The Rho-kinase dependency of contractions induced by exogenously applied prostaglandin F2α (PGF2α) and prostaglandin E2 (PGE2) was also studied. In addition, the effects of the selective FP-receptor antagonist AL-8810 (10 μM) and the selective EP1-antagonist AH-6809 (10 μM) on growth factor-induced contractions were investigated, both in intact and epithelium-denuded preparations. Growth factor-induced PGF2α-and PGE2-release in the absence and presence of Y-27632, U-0126 and indomethacin, was assessed by an ELISA-assay.Results
Epidermal growth factor (EGF)-and platelet-derived growth factor (PDGF)-induced contractions of guinea pig tracheal smooth muscle preparations were dependent on Rho-kinase, MAPK and COX. Interestingly, growth factor-induced PGF2α-and PGE2-release from tracheal rings was significantly reduced by U-0126 and indomethacin, but not by Y-27632. Also, PGF2α-and PGE2-induced ASM contractions were largely dependent on Rho-kinase, in contrast to other contractile agonists like histamine. The FP-receptor antagonist AL-8810 (10 μM) significantly reduced (approximately 50 %) and the EP1-antagonist AH-6809 (10 μM) abrogated growth factor-induced contractions, similarly in intact and epithelium-denuded preparations.Conclusion
The results indicate that growth factors induce ASM contraction through contractile prostaglandins – not derived from the epithelium – which in turn rely on Rho-kinase for their contractile effects. 相似文献16.
Three 16-aryloxy analogues of PGF2α are potent, full agonists on the isolated rabbit jejunum. Their actions are more prolonged than that of PGF2α, and radioactive tracer studies with one of the analogues reveal a slower wash-out of the analogue compared to PGF2α, under superfusion conditions. During the prolonged contractile response diminished responses to PGF2α were obtained: this effect was investigated in terms of receptor desensitization. The actions of these analogues were also investigated on the isolated guinea-pig ileum and the rabbit oviduct
. 相似文献
17.
Douglas W.P. Hay Roseanna M. Muccitelli Derek L. Hortsmeyer David Raeburn 《Prostaglandins & other lipid mediators》1988,35(4)
To examine further the possible prostanoid involvement in the influence of the epithelium on guinea-pig tracheal smooth muscle responsiveness, we have analyzed the effects of LTD4, methacholine and histamine on the level of airway smooth muscle tone and on the amounts of PGE2α and PGI2 (determined by radioimmunoassay) in the presence and absence of the epithelium. Removal of the epithelium increased the sensitivity of guinea-pig trachea to the contractile effects of LTD4, methacholine and histamine. LTD4 (3–100 nM), methacoline (0.1–10 μM) or histamine (0.3–30 μM) did not increase prostanoid release above control values in either the presence or absence of the epithelium. The unstimulated release of PGE2 and PGF2α but not PGI2, was decreased in tissues lacking epithelium. Indomethacin (1 μM) reduced the baseline tone to a smaller extent in the absence of epithelium. In the presence but not the absence of the epithelium, indomethacin increased the sensitivity of preparations to the contractile effect of methacholine. The results support the postulate of an epithelium-derived inhibitory factor modulating guinea-pig tracheal smooth muscle responsiveness. The identity of this factor is not known but is not PGI2 and is unlikely to be PGF2α or PGE2. However, the possibility remains that the basal release of PGE2 and/or PGF2α derived from the epithelium may markedly affect the responsiveness of guinea-pig tracheal smooth muscle. Furthermore, the epithelium is a significant source of PGE2 and PGF2α which may be involved in the maintenance of baseline tone. 相似文献
18.
T. Laudanski M.D. Ph.D. A. Kostrzewska Ph.D. kerlund 《Prostaglandins & other lipid mediators》1986,32(1)
The effect of cupric ions on the human uterus and the involvement of prostaglandins (PGs) in mediating this effect was studied by recording of isometric contractions of isolated myometrial strips and pieces of uterine arteries, and by intrauterine pressure recordings in women before the onset of menstruation.
, CuCl2 in concentrations of 10−4 M and higher caused a significant inhibition of myometrial contractile activity, but no effect on the artery preparations was seen. Furthermore, the contractile response of myometrial strips to PGF2α and PGE2 (10 ng/ml) decreased in the presence of CuCl2 in concentrations of 5 and 50 μmol.
, instillations of 0.3, 1.0 and 2.0 mM of CuCl2 in 0.7 ml of saline solution into the uterine cavity caused a dose-dependent stimulation of uterine activity, but after pretreatment with naproxen, 500 mg orally, the effect of these substances was abolished. After naproxen treatment, but during infusion of PGF2α (5 μg/min), the response to the CuCl2 solutions was partially restored. It is suggested that cupric ions, at high concentrations, have an inhibiting effect on myometrial activity. The stimulatory effect of low doses of CuCl2 seen after installation into the uterine cavity is largely exerted via initiation of synthesis and release of endometrial PGs. 相似文献
19.
Induction of 20α-hydroxysteroid dehydrogenase in rat corpora lutea of pregnancy by prostaglandin F2α
20α-OH-SDH is a marker of luteolysis in rat corpora lutea and appearance of this enzyme is inhibited by prolactin but stimulated by LH or hCG. PGF2α induced 20 α-OH-SDH activity in corpora lutea of pregnant rats and a significant fall in peripheral plasma progesterone concentrations when administered i.m. for two consecutive days. Rats treated with PGF2 α on days 8 and 9 of pregnancy were resorbing implants by day 10. Exogenous progesterone, but not estrogen, prevented implant resorption, yet 20 α-OH-SDH appeared in the corpora marking luteolysis. HCG, LH and prolactin, but not FSH, prevented pregnancy termination and inhibited induction of 20 α-OH-SDH in rats treated with PGF2 α in early pregnancy. PGF2α also induced 20α-OH-SDH in luteal tissue of intact and hypophysectomized rats treated on days 14 and 15 of pregnancy, but neither exogenous steroids or gonadotrophins blocked the induction of the enzyme in rats treated at this time. The increase in lutein 20α-OH-SDH activity during the peripartal period was partially blocked by administration of the prostaglandin biosynthesis inhibitor, indomethacin, suggesting a role for endogenous prostaglandins in the induction of 20α-OH-SDH at term. It appears that PGF2α acts directly on the ovary to induce 20α-OH-SDH activity by preventing the luteotrophic action of prolactin. Other luteal NADPH-dependent dehydrogenase activities are not markedly stimulated following PGF2α administration. 相似文献
20.
Pregnant hamsters were administered (SC) prostaglandin or vehicle on the morning of the 4th day of pregnancy. Serum progesterone was significantly depressed (p<.01) at 0.5, 2, and 6 hours after treatment with 100 μg PGF2α. Serum progesterone levels were unchanged 2 hours and 6 hours after treatment with 100 μg PGF2β and 2 hours after treatment with 1 mg PGF2β. Progesterone levels were depressed to less than 1 ng/ml 6 hours after treatment with 1 mg PGF2β. The specific uptake of 3H-PGF2α in whole hamster corpora lutea was significantly depressed 2 hours and 6 hours following 100 μg PGF2α treatment. A 15% depression in specific uptake occurred 0.5 hour post-treatment. Treatment with 100 μg PGF2β resulted in no change. Administration of 1 mg PGF2β resulted in depressed 3H-PGF2α uptake at both 2 and 6 hours post-treatment.Prostacyclin (PGI2) treatment resulted in no change in either 3H-PGF2α specific uptake or serum progesterone 2 hours after 100 μg treatment SC. These parameters were both reduced approximately 30% 6 hours post-treatment. Treatment with 6-keto-PGF1α resulted in a complete lack of measurable 3H-PGF2α uptake and serum progesterone levels less than 1 ng/ml at both 2 and 6 hours after treatment with 1 mg SC. 相似文献