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1.
Burkhard Scherer Jürgen Schnermann Mike Sofroniev Peter C. Weber 《Prostaglandins & other lipid mediators》1978,15(2):255-266
Thw radioimmunological (RIA) determination of prostaglandin (PG) E2 and of PGF2α in urine humans and rats is described in detail. After extraction and chromatography PGE2 was determined by using a PGE specific antibody or by using either PGB or PGF2α specific antibodies after the respective conversion procedures. The three different RIA procedures were compared to each other. PGF2α was determined by a specific antibody to PGF2α. Basal excretion of PGE2 and of PGF2α in healthy women on free diet was 9.3 ng/hour ± 0.96 and 18.3 ng/hour ± 2.5 respectively. Furosemide increased the excretion of PGE2 and of PGF2α in humans significantly, while PG-excretion rates decreased on indomethacin. In rat urine PGE2 and PGE2α increased markedly from 46.2 pg/min ± 9.3 and 27 ± 3.4 to 253.8 ± 43.3 and 108 ± 12.6 pg/min (per one kidney) in the anesthetized-laparotomized animal. This increase was abolished after giving two different PG synthetase inhibitors. 相似文献
2.
G.J. Wiepz M.C. Wiltbank S.B. Kater G.D. Niswender H.R. Sawyer 《Prostaglandins & other lipid mediators》1993,45(2)
When ovine large luteal cells are placed in culture and exposed to PGF2α, there is a rapid and sustained increase in the concentration of free intracellular calcium which is believed to play a major role in the luteolytic and cytotoxic effects of PGF2α. Since administration of exogenous PGE2 can prevent spontaneous and PGF2α-induced luteolysis in vivo, and the cytotoxic effects of PGF2α on large luteal cells in vitro, the objective of this study was to determine if one mechanism by which PGE2 acts is to attenuate increases in free intracellular calcium induced by PGF2α. At concentrations of 10 nM or greater, PGF2α caused a significant and sustained increase in free intracellular calcium in large luteal cells. Similarly, PGE2 also induced increases in free intracellular calcium but required doses 20-fold greater than PGF2α. When PGE2 (1, 10 or 100 nM) was incubated with PGF2α (100 nM) increases in free intracellular calcium induced by PGF2α were attenuated (P<0.05) when measured 5 min, but not at 30 min, after initiation of treatment. The observed decrease in the concentration of free intracellular calcium at 5 min in response to PGF2α was the result of fewer cells responding to PGF2α. In addition, the concentrations of free intracellular calcium attained in the cells that did respond was reduced 25% compared to cells treated with PGF2α alone. Thus, part of the luteal protective actions of PGE2 appears to involve an inhibition of the early (5 min) increase in free intracellular calcium induced by PGF2α. 相似文献
3.
To evaluate the details of the adrenergic stimulation of urinary prostaglandins in man, ten normal volunteers were given various agonists and antagonists. The effect of 4 hour IV infusions of norepinephrine (NE), NE + phentolamine (PHT), NE + phenoxybenzamine (PHB), NE + prazosin (PZ), isoproterenol (ISO), and PHT alone on urinary PGE2 and PGI2 (6 keto PGF1α) were determined. PGE2 and 6 keto PGF1α were measured by radioimmunoassay from 4 hour urine samples. NE stimulated both PGE2 (196±40 to 370±84 ng/4 hrs/g creatinine and 6 keto PGF1α(184±30 to 326±36), both p<0.01. In contrast, ISO had no effect on either PGE2 or 6 keto PGF1α excretion. Alpha blockade with PHT. PHB, or PZ inhibited the NE induced systemic pressor effect. However, the effect of the alpha blockers on the NE induced stimulation of PGE2 and 6 keto PGF1α varied. PHT did not alter the NE stimulated PGE2 or 6 keto PGF1α release (370±84 vs. 381±80) PGE2 and (326±50 vs. 315±40) 6 keto PGF1α, both p>0.2). PHT alone stimulated only 6 keto PGF1α. PHB and the specific α1 antagonist PZ similarly eliminated the NE induced prostaglandin release. These results suggest that adrenergically mediated urinary prostaglandin release in man is via an alpha receptor with α1 characteristics. 相似文献
4.
Ryo Kawata Yoshihiro Urade Masayoshi Tachibana Osamu Mizukoshi 《Prostaglandins & other lipid mediators》1988,35(2)
The exogenous and endogenous syntheses of prostaglandins (PG's) by the cochlea of adult mongolian gerbils were studied
. After incubation of the whole membraneous cochlea with [3H]-arachidonic acid (AA), syntheses of PGF2α, 6-keto PGF1α, PGE2, thromboxane (TX) B2 and PGD2 were evidenced in this order. The synthesis of radioactive PG's was almost completely inhibited by incubation with 10−5 M indomethacin. No significant amounts of those PG's were detected by radioimmunoassay (RIA) in the cochlea obtained from animals killed by microwave irradiation at 5.0 kw for 0.8 sec. However, when the homogenate of the whole membraneous cochlea obtained from animals without microwave irradiation was incubated at 37°C for 0–15 min, PGD2, PGE2, PGF2α and 6-keto PGF1α were found to be formed from endogenous AA in the cochlea by RIA. PG's were formed already at 0 time to considerable level (PGD2, PGF2α and 6-keto PGF1α, 90–120 pg/cochlea; PGE2, 370 pg/cochlea), reached to the maximum level (PGD2, PGF2α and 6-keto PGF1α, 170–200 pg/cochlea; PGE2, 500 pg/cochlea) at a 5-min incubation, and then gradually decreased. On the other hand, the amount of TXB2 was lower than the detection limit by RIA (<50 pg/cochlea) even after the incubation. The cochlea was dissected into three parts: organ of Corti + modiolus (OC + M), lateral wall (LW), and cochlear nerve (CN), and then PG's formed by these tissues were determined after a 5-min incubation of the homogenates. In the CN and OC + M, PGE2 was the major PG (100 and 160 pg/tissue, respectively), and the amounts of PGD2, PGF2α and 6-keto PGF1α were about
of those of PGE2. In the LW, the amounts of PGD2, PGE2, PGF2α and 6-keto PGF1α were about the same level (70–100 pg/LW). 相似文献
5.
L.A. Reichard H.D. Hafs N.B. Haynes R.J. Collier T.E. Kiser M.S. McCarthy 《Prostaglandins & other lipid mediators》1978,16(1):135-142
Two experiments were conducted, the first to compare sperm output and the second to determine serum testosterone in rabbits given PGF2α or PGE2. In the first, six rabbits were ejaculated twice each Monday, Wednesday and Friday for 5 weeks. Each rabbit was given subcutaneously (sc) each of the following treatments five times: 1) saline, 2) 5 mg PGF2α and 3) 5 mg PGE2. Treatments were given, half at 4 hr and half at 2 hr before first ejaculations. Both PGF2α and PGE2 caused increased (50% and 84%) sperm content of first ejacula, without significantly altering characteristics of second ejacula. The extra sperm in first ejacula was a function of increased sperm density, because seminal volume was unaltered.In the second experiment, 15 rabbits were bled at 0.5-hr intervals for 9 hr and given (sc): 1) saline at 1 and 3 hr (n=4), 2) 2.5 mg PGF2α at 1 and 3 hr (n=4), 3) 2.5 mg PGE2 at 1 and 3 hr (n=4) or 4) 5 mg PGF2α at 1 hr after the onset of blood sampling. In saline-treated controls, episodic surges of testosterone occurred on the average every 5 hours. After the injection of 2.5 or 5.0 mg PGF2α, serum testosterone began to rise at 0.5 hr, peaked (8 to 13 ng/ml) at 1 hr and approached a nadir (0.5 ng/ml) within 4 hours. The second injection of 2.5 mg PGF2α failed to significantly affect serum testosterone. PGE2 treatment was followed by significantly depressed serum testosterone; only 1 of these 4 rabbits had any surge of testosterone for the 8 hr after treatment. In conclusion, PGF2α and PGE2 both increased sperm output, but PGF2α increased serum testosterone while PGE2 depressed serum testosterone. Thus, the sperm output effect of these prostaglandins probably is independent of the acute changes in testosterone secretion. 相似文献
6.
High pressure liquid chromatography (HPLC) using 4′ × 1/8″ columns of a pellicular silica support (Corasil-II) allows identification of prostaglandins diastereomers based on their characteristic retention relative to a standard, PGE2 in this study. Surprisingly this simple method allows separation of PGE2, PGE1, and PGEo (dihydro-PGE1) or PGF2α, PGF1α, and PGFoα without resort to silver nitrate impregnated stationary phases. Even more subtle distinctions such as that between 13,14-dihydro-PGF2α, PGF1α and 5,6-
-PGF2α are possible by HPLC. The differential refractometer detector used throughout can also be used for quantitation. This is illustrated by a study of the relative rates of degradation of natural PGF2α (an oil at the temperature employed, 41°C) and racemic PGF2α (mp. 63°) on exposure to air. 相似文献
7.
Four antiestrogens (anordiol, tamoxifen, RU 39411, ICI 182780) and the antiprogestin, mifepristone (RU 486), were administered to the following three animal models: (1) ovariectomized rats, (2) mated rats treated post-coitally; and (3) pregnant rats treated post-implantation. The antiestrogens were administered alone or in combination with mifepristone at doses effective in preventing and/or terminating pregnancy in rats. The objective of the study was to determine whether these drugs influenced uterine concentrations of prostaglandins (PGF2α and PGE2).Antiestrogens administered alone to ovariectomized rats did not effect uterine PGE2 or PGF2α concentrations; whereas the combination of anordiol/mifepristone increased uterine PGF2α concentration, resulting in an increase in the PGF2α/PGE2 ratio.Mated rats were treated post-coitally for three consecutive days with anordiol, tamoxifen, estradiol and mifepristone alone and with the combination of anordiol/mifepristone and tamoxifen/mifepristone. An increase in uterine PGF2α concentrations and in the PGF2α/PGE2 ratio occurred only in anordiol/mifepristone treated group. A decrease in uterine PGE2 concentrations occurred in animals treated with anordiol, tamoxifen and estradiol, resulting in an increase in the PGF2α/PGE2 ratio.Anordiol (5.0 mg/kg/day) and mifepristone (4.0 mg/kg/day) alone and the combination of anordiol/mifepristone (2.5/1.0 mg/kg/day) administered to pregnant rats on days 7, 8 and 9 of pregnancy induced an increase in PGF2α levels without affecting uterine PGE2 concentration. The changes in uterine PGF2α concentrations induced by anordiol and the combination of anordiol/mifepristone resulted in an increase in the PGF2α/PGE2 ratio.The antiestrogens tested except for ICI 182780 possessed agonist activity when assayed by measuring their capacity to increase the uterine weights in ovariectomized rats. Also, ICI 182789 was the only antiestrogen that did not influence uterine PG concentrations. It can be concluded that ICI 182780 is the only “pure” antiestrogen among those tested.The present results show that antiestrogens and the combination of mifepristone plus anordiol at doses preventing implantation and terminating pregnancy increase uterine PGF2α and/or decrease PGE2 concentrations, resulting in an alteration of PGF2α/PGE2 ratio. These findings suggest that there exists a critical balance of PGF2α to PGE2 concentrations in the uterus required for the normal passage of fertilized ova through the oviduct, initiating implantation of the blastocysts, development of embryos, and maintenance of pregnancy. 相似文献
8.
The receptors mediating prostanoid-induced contraction of guinea-pig isolated trachea have been characterised in terms of a recently proposed general classification of prostanoid receptors. Results obtained on the trachea were compared with those obtained on guinea-pig fundus, which contains a sub-type of PGE2-sensitive (EP-) receptor termed the EP1-receptor, and guinea-pig lung strip, which contains a thromboxane-sensitive or TP-receptor. The following agonists were studied, PGE2, PGF2α and the thromboxane-like agonists U-46619 and Wy17186. The antagonists studied were SC-19220 which selectivity blocks EP1-receptors, and AH19437 which selectively blocks TP-receptors. On guinea-pig fundus the rank order of agonist potency was PGE2 > PGF2α > Wy17186 U-46619, and responses to all agonists were antagonised by SC-19220 but not by AH19437. On guinea-pig lung strip the rank order of potency was U-46619 > Wy17186 PGF2α > PGE2 and responses to all agonists tested were blocked by AH19437 but not by SC-19220. On the trachea, the rank order was PGE2 = U-46619 > Wy17186 = PGF2α. SC-19220 antagonised responses to PGE2 and PGF2α, but not those to U-46619 or Wy17186. Conversely, AH19437 antagonised responses to U-46619 and Wy17186 but not those to PGE2 or PGF2α. It is concluded that prostanoid-induced contractions of guinea-pig trachea can be mediated by both EP1- and TP-receptors. 相似文献
9.
D. M. Grennan I. J. Zeitlin W. S. Mitchell W. W. Buchanan W. C. Dick 《Prostaglandins & other lipid mediators》1975,9(5):799-816
In these experiments we have examined the effects of PGE1, PGE2, PGF1α and PGF2α on synovial perfusion in the normal canine synovial microcirculation. The effects of the drugs on synovial perfusion were determined indirectly from the changes produced in the rate of clearance of 133Xenon from the joint by their intra-articular injection. Prostaglandins PGE1 and PGE2 were found to be strongly vasodilator with PGE1 being the more active. PGF1α appeared to have little or no vasoactive properties in doses up to 1 ugm. (2.8 × 10−5M) in our I preparation while PGF2α was vasodilator at this high dosage only. Neither SC19920 nor diphloretin phosphate antagonised the effects of PGE1 in these experiments. 相似文献
10.
C. H. Spilman 《Prostaglandins & other lipid mediators》1974,7(6):465-472
Oviductal motility was measured in the isthmus of ovariectomized New Zealand rabbits. The effects of estradiol and progesterone on spontaneous motility and on the response of the oviduct to exogenously administered prostaglandin E1 (PGE1) and PGF2α were determined. Estradiol treatment significantly increased both the amplitude (P<0.05) and frequency (P<0.01) of spontaneous contractions. The amplitude of spontaneous activity was less following progesterone treatment than following estradiol treatment (P<0.05). Progesterone treatment increased the duration of oviduct response to PGE1 (P<0.05). Estradiol treatment had no effect on the response to PGE1. Increased oviductal activity caused by PGF2α lasted significantly (P<0.01) longer in ovariectomized, untreated animals than in ovariectomized animals treated with estradiol or progesterone. Progesterone was more effective than estradiol in decreasing the duration of the response to PGF2α. These effects of steroid hormones on the responsiveness of the oviduct to PGE1 and PGF2α could contribute to the physiological control of egg transport. The nadir of ovarian hormone influence, as in the recently ovariectomized animals and as occurs immediately after ovulation, is associated with a high responsiveness of the oviduct to PGF2α. This could effectively increase isthmic occlusion and prevent the eggs from passing through the oviduct prematurely. The gradual increase in ovarian estradiol and progesterone secretion during the 3
days following coitus could result in decreased responsiveness to PGF2α and increased responsiveness to PGE1. These changes might cause relaxation of isthmic tone and allow movement of eggs through the isthmus into the uterus. 相似文献
11.
H. Thaler-Dao M. Saintot M. Ramonatxo C. Chavis A.Crastes de Paulet 《Prostaglandins & other lipid mediators》1982,23(3):347-359
Prostaglandin biosynthesis was studied in the rat uterus during the oestrous cycle. Uterine homogenates were incubated for 20 minutes in the presence of exogenous substrate (2.10−5M). PGF2α and PGE2 were measured by R.I.A.. A sharp peak PGF2α and a smaller peak of PGE2 were observed at prooestrus, 20 h. Another small PGE2 peak occurred at dioestrus II, 15 h. The lowest values of both PGs were found on dioestrus, 15 h. Plasma oestradiol concentration were highest at proestrus, 15 h and 20 h. A sharp progesterone peak occurred at prooestrus, 20 h. The PGF2α peak is next to the oestradiol peak and is superimposable or lags slightly beyond the progesterone peak.Incubation with 14C arachidonic acid and subsequent analysis of extracts by TLC and scanning showed that the major metabolite is PGI2, identified as 6 keto PGF1α. The conversion rate of arachidonic acid into 6 keto PGF1α is 5 times higher than into PGF2α. 6 keto PGF1α was further identified by GC/MS. No significant difference was observed between 6 keto PGF1α production during oestrus and dioestrus. 相似文献
12.
Background
Eicosapentaenoic acid-derived prostaglandin (PG) E3, PGF3α, and thromboxane (TX) B3 are bioactive lipid mediators which have anti-cancer and anti-inflammatory effects. To exert their effects, PGE3, PGF3α, and TXB3 must be released to the extracellular space from cells, but the release mechanism has been unclear. We therefore investigated the contribution of ATP-binding cassette transporter C4 (ABCC4), which has been known as a prostanoids efflux transporter, to the release of PGE3, PGF3α, and TXB3.Materials and Methods
ATP-dependent transport of PGE3, PGF3α, and TXB3 via ABCC4 was investigated by using inside-out membrane vesicles prepared from ABCC4-overexpressing HEK293 cells. To evaluate the contribution of ABCC4 to the release of PGE3, PGF3α, and TXB3, we measured the extracellular and intracellular levels of PGE3, PGF3α, and TXB3 in A549 cells when we used ABCC4 inhibitors (dipyridamole, MK571, and probenecid) or ABCC4 siRNAs. The quantification of PGE3, PGF3α, and TXB3 was performed by using liquid chromatography-tandem mass spectrometry.Results
The apparent Km values for ABCC4-mediated transport were 2.9±0.1 µM for PGE3, 12.1±1.3 µM for PGF3α, and 11.9±1.4 µM for TXB3 and the ATP-dependent accumulation of PGE3, PGF3α, and TXB3 into vesicles was decreased by using typical substrates and inhibitors of ABCC4. ABCC4 inhibitors and ABCC4 knockdown showed the reduction of extracellular/intracellular ratio of PGE3 (40–60% of control) and PGF3α (60–80% of control) in A549 cells.Conclusions
Our results suggest that PGE3, PGF3α, and TXB3 are substrates of ABCC4 and ABCC4 partially contributes to the release of PGE3 and PGF3α. 相似文献13.
Lawrence Levine Kung-Yue Wu Sheng-Shung Pong 《Prostaglandins & other lipid mediators》1975,9(4):531-544
Antibodies directed toward PGF2β were prepared in rabbits. The serologic specificity of the immune reaction was determined by inhibition of sodium borohydride-reduced (3H) PGE2 anti-PGF2β binding by several prostaglandins. The antibodies to PGF2β recognize the β-hydroxyl configuration in the cyclopentane ring of PGF2β. With the use of both anti-PGF2α and anti-PGF2β, the product of PGE2 reduction by 9-ketoreductase purified from chicken heart was identified as PGF2α. Guinea pig liver and kidney homogenates were examined for PGE 9-ketoreductase activity. Although enzyme activity was present, no evidence of PGF2β production was found. 相似文献
14.
A method for the evaluation of PGF2α and PGE2 biosynthesis in rat cerebral cortex is described. Tissue slices were incubated without any added precursor for different lengths of time. The analytical procedure involves prostaglandin extraction, purification and quantitative determination by mass fragmentography. Significant amounts of both prostaglandins were synthesized. The biosynthesis reached a plateau after 30 minutes and the ratio of PGF2α to PGE2 was approximately 3. 相似文献
15.
Prepubertal gilts given 750 IU pregnant mares′ serum gonadotropin (PMSG) followed 72 h later by 500 IU human chorionic gonadotropin (hCG) to induce follicular growth and ovulation fail to ovulate when 10 mg/kg indomethacin (INDO) is injected 24 h after hCG administration. This study examines the effects of administration of exogenous prostaglandins F2α and E2 (PGF2α and PGE2) alone or in combination, and at various times prior to the expected time of ovulation, on the INDO blockade of ovulation in PMSG/hCG-treated gilts. Occurrence of ovulation was determined by visual observation at laparotomy 48 h after hCG. When 5 mg or 10 mg PGF2α was injected at each of 38, 40 and 42 h after hCG injection, 63% and 79%, respectively, of preovulatory follicles ovulated. In contrast, injection of 5 mg PGE2 or 5 mg PGE2 plus 5 mg PGF2α induced ovulation in 0% and 24% of preovulatory follicles, respectively. In control groups, 100% of folicles in PMSG/hCG-treated gilts ovulated whereas none did so in PMSG/hCG/INDO-treated animals. These results indicate that administration of PGF2α can induce ovulation in the PMSG/hCG/INDO-treated prepubertal gilt and suggest that PGE2 is ineffective and may be antagonistic to PGF2α in overcoming the ovulation blocking effect of INDO. 相似文献
16.
Anders gmo 《Prostaglandins & other lipid mediators》1975,9(3):451-457
PGE1(50μg/animal) and PGF2α (250 μg/animal) caused a transient in serum LH at 5 min after injection. PGE1 (250 μg/animal) had a biphasic effect on serum LH. A small peak was obtained at 5 min, and a second, larger peak at 60 min after injection. It is suggested that the first peak is a result of the stress associated with injection of the PGs, whereas the second peak represents a physiological effect of PGE. Subcutaneous injection of PGE1 (1 mg in arachis oil b.i.d.) for 10 days did not affect the concentration of LH in serum, the function of the accessory sexual glands or the sexual activity. PGF2α, given at the same dose and in the same manner, increased the sexual activity but left all other variables unaffected. The pituitary responsiveness to LH-RH was unaltered by the treatment with PGE1 and PGF2α. 相似文献
17.
The results of the present study establish that 1.5 mg PGE2 (lyophilized sodium salt) incorporated in one cm long open-ended Silastic-polyvinylpyrrolidone (PVP) tube when inserted into 10 day pregnant rats induced abortion within 70–72 hours in all the treated rats. A combined treatment of PGE2 and 17β-estradiol failed to increase the abortion inducing effect of a Silastic-PVP-PGE2 tube. It is observed that PGE2 is about 4 times less potent than PGF2α in inducing midterm abortion in rats. It is suggested that either PGE2 exerts luteolytic effect after being converted
to PGF2α, although how it occurs is not clear; or PGE2 causes expulsion of the fetuses by its uterine stimulating property. 17β- estradiol increases the uterine synthesis of PGF2α as described earlier but seems not affecting the production of PGE2 by the uterus. The release rate of 3H-PGE2 from Silastic-PVP tube
and
is also described. 相似文献
18.
The role of progesterone in regulation of uteroovarian venous concentrations of prostaglandins F2 α (PGF2α) and E2 (PGE2) during days 13 to 16 of the ovine estrous cycle or early pregancy was examined. At estrus, ewes were either mated to a fertile ram or unmated. On day 12 postesturus, ewes were laparotomized and a catheter was inserted into a uteroovarian vein. Six mated and 7 unmated ewes received no further treatment. Fifteen mated and 13 unmated ewes were ovariectomized on day 12 and of these, 7 mated and 5 unmated ewes were given 10 mg progesteron sc and an intravaginal pessary containing 30 mg of progesterone. Uteroovarian venous samples were collected every 15 min for 3 h on days 13 to 16 postestrus. Mating resulted in higher mean daily concentrations of PGE2 in the uterovarian vein than in unmated ewes. Ovariectomy prevented the rise in PGE2 with day in mated ewes but had no effect in unmated ewes. Progesterone treatment restored PGE2 in ovariectomized, mated ewes with intact embros. Mating had no effect on mean daily concentrations of PGF2α or the patterns of the natural logarithm (ln) of the invariance of PGF2α. Ovariectomy resulted in higher mean concentrations and ln invariances of PGF2α on day 13 and lower mean concentrations and ln invariances of PGF2α on days 15 and 16. Replacement with progesterone prevented these changes in patters of mean concentrations and ln variances of PGF2α following ovariectomy. It is concluded that progesterone regulates the release of PGF2α from the uterus, maintaining high concentrations while also preventing the occurrence of the final peaks of PGF2α which are seen with falling concentrations of progesterone. This occurs in both pregnant and non-pregnant ewes. Progesterone is also needed to maintain increasing concentrations of PGE2 in mated ewes. 相似文献
19.
The mechanism of the stimulatory effect of prostaglandin (PG) F2α on the production of hexosamine-containing substances by cultured fibroblasts was studied with special reference to adenosine 3′:5′- cyclic monophosphate (cAMP). At the stationary phase, the cells were exposed for 6 hrs to PGF2α, E1, cAMP or dibutyryl-cAMP in a wide range of concentrations. cAMP itself showed a slight stimulation on the production of hexosamine-containing substances, and the effect was enhanced by using the dibutyryl derivative. PGF2α had much a greater capacity than either the exogeneous cAMP or the dibutyryl-cAMP for enhancing the production of hexosamine-containing substances. To know whether cAMP is involved in the stimulatory effect of PGF2α, intracellular cAMP level was concomitantly measured in both PGF2α and PGE1 treated cultures. Although the cellular cAMP level in PGE1 treated cultures was much higher than that in the PGF2α treated cultures, the stimulatory effect on the production of hexosamine-containing substances in PGE1 treated cultures was always much smaller than that in the PGF2α treated cultures. Moreover, PGF2α had a significant stimulatory effect on the production of hexosamine-containing substances even at a low concentration as 100 pg/ml, which is small enough not to increase any cellular cAMP level. From these results, it was concluded that the stimulatory effect of PGF2α on the production of hexosamine-containing substances by cultured fibroblasts is not mediated by cAMP and is caused by a mechanism different from that caused by cAMP. 相似文献
20.
Three prostaglandins (PGF2α and PGE1, PGE2) have been found in maternal and fetal circulation during labour. Two of these prostaglandins (PGF2α and PGE2) are present in elevated levels in maternal circulation during labour and their presence in fetal vessels has been shown.These three prostaglandins have been tested for their effects on fetal vessels in vitro (umbilical artery and vein, ductus arteriosus, and smaller pulmonary artery). These vessels were selected as being crucial in the conversion from fetal to extra-uterine circulation in mammalian species. Responses of these vessels to the prostaglandins under varying oxygen regimes have been examined as well as their responses to prostaglandin inhibitors. Activity of vessels of varying gestational ages exposed to PGF2α was also examined. The following results were obtained:
- 1. All vessels, with the exception of pulmonary arteries, contracted in the presence of oxygen over the range 20–100mmHg pO2. At a pO2 of < 20mmHg the ductus arteriosus remained inactive or dilated. Pulmonary arteries dilated at high pO2.
- 2. All vessels contracted in response to exogenous PGF2α with the exception of the pulmonary arteries which dilated. In the presence of PGF2α, the umbilical veins dilated under low (< 20mmHg) pO2 and contracted at higher levels. Contraction also occurred at lower levels after a period of time.
- 3. Although PGF2α was capable of causing contraction in the ductus arteriosus at near zero pO2, oxygen, (or possibly the products of oxygenation), appear to be required for continued contraction in the presence of PGF2α. A synergistic relationship between oxygen and PGF2α responses was found as oxygen tensions increased. A synergistic response between PGF2α and oxygen with umbilical arteries which did not increase with increased pO2 was also found. Oxygen tension appeared to have little effect on the response of other vessels to PGF2α.
- 4. PGE1 caused dilations in all vessels examined. Such dilations appearing to be independent of the oxygen regime prevailing. However, an increase in oxygen during experiments reversed any dilation caused by the prostaglandins.
- 5. PGE2 caused contractions in umbilical vessels which were independent of oxygen. PGE2 caused contraction of pulmonary arteries. However, in the ductus arteriosus, PGE2 caused an initial contraction followed by a strong dilation. This dilation became weaker as pO2 increased.
- 6. Additions of prostaglandin inhibitors (Naproxen and Indomethacin) to the bathing solution in which the ductus arteriosus and umbilical arteries were contracting (in response to PGF2α, or oxygen alone) caused a decrease in contractions, and sometimes a slight decrease when the vessel had been pretreated with PGF2α suggesting a possible need for endogenously synthesised prostaglandins for the maintenance of oxygen mediated contractions (in vivo).
- 7. Vessels responsed to PGF2α at an early gestational age. A role for prostaglandins and oxygen in the closure of fetal vessels is discussed.