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1.
M S Kim  Y L Lee  Y H Jo  S S Sim  H Choi 《Prostaglandins》1985,30(1):99-107
Prostaglandins (PGs) are believed to be present in the gastrointestinal tract and to increase the tone of longitudinal muscle layer. However the influence of PGs on the gastric slow wave (SW) is not clarified yet. We therefore investigated the effect of prostaglandin E2 (PGE2) on the electrical and the mechanical activities of feline isolated stomach muscle strips (7 X 1.5 cm), using five capillary electrodes (Ag-AgCl) and an isometric force transducer connected to the antral edge. One hundred and ninety-six strips, obtained from the corpus and antrum of 196 anaesthetized cats, were studied in a muscle chamber filled with Krebs solution (pH 7.4, temperature 36 degrees C) bubbled with 5% CO2 in O2. Exogenous PGE2 concentration-dependently increased the gastric SW frequency without affecting the spike and mechanical activities. Indomethacin decreased the SW frequency. These responses to PGE2 or indomethacin were not blocked by phentolamine, propranolol, hexamethonium, atropine or tetrodotoxin. It is therefore suggested that PGE2 facilitates the development of the gastric SW by an action on the muscle that does not involve cholinergic or adrenergic mechanism.  相似文献   

2.
The contracting and relaxing potencies of anf interactions between a number of prostaglandins (PGs) were studied in vitro on spiral strips of small canine mesenteric arteries (outside diameter < mm). PGF2α and PGE2, the most potent contracting PGs, were nearly equal in potency (EC50 4 × 10?7M) and did not cause relaxation under our experimental conditions. PGI2 and PGE1 were equal and the most potent relaxing PGs (EC50 3 × 10?9M). PGE1 also caused contraction, but this effect was not consistent. PGI2 did not cause contraction in concentrations up to 3 × 10?6M. In higher concentrations, however, it caused abrupt and near maximal contraction. PGD2 was weak in both respect, causing incomplete relaxation and contraction or biphasic effects. Interaction studies showed that PGE1 and PGI2 mutually excluded the relaxing effects of each other. PGE1 also reversed the relaxing effect of isoproterenol. However, pre-exposure to PGD2 did not attenuate the relaxing effect of PGE1 or PGI2 nor was the relaxing effect of PGD2 changed by pre-exposure to PGE1. Two different orders of potency of PGs suggest two PG receptors subserving contraction and relaxation, respectively. Further, it appears that several PGs can act upon both receptors which may explain unusual interactions between the PGs and some of their atypical effects. Finally, the data also suggest that there may be subtypes of the PG receptors subserving contraction and relaxation.  相似文献   

3.
Prostaglandins (PGs) E1 or F (1.4−8.4 × 10−8 M) contracted strips of rabbit aorta and increased the contractions produced by 1−6 × 10−7 M phenylephrine (PE). The addition of the PGs simultaneously with PE or after a low concentration of PE (2 × 10−7 M) significantly increased the PE-induced contractions. However, when the PGs were added after a higher concentration of PE (6 × 10−7 M) an additional increase in the PE-induced contraction was produced with PGF but not with PGE1. Isobolic plots of the data obtained from the simultaneous addition of PE and the PGs indicate that both PGs interact with PE in a synergistic or potentiative manner, suggesting that their effects are mediated through different receptor mechanisms. Addition of the PGs after a high dose of PE indicates that there may also be either qualitative or quantitative differences between PGE1 and PGF.  相似文献   

4.
Prostaglandins E1 (PGE1) and E2 (PGE2) have been coupled with the amine group of phosphatidylethanolamine (PE) by means of dicyclohexylcarbodiimide. These complexes basically mimic the relaxant and contractile effects of the corresponding free prostaglandins (PGs) on various smooth muscle preparations, but exhibit a delayed onset of action and a lower affinity for the PG receptors. The complexes are comparable with the free, parent PGs, in their intrinsic activities. The same holds true for the effects on blood pressure and on the motility of the uterus . The PGE2-PE complex is hydrolysed to release obviously free PGE2 by cell-free homogenates prepared from various tissues, but not by blood plasma. The PGE2-PE complex is immunologically indistinguishable from the free PGE2.  相似文献   

5.
The presence of prostaglandins (PGs) was determined in gastric juice obtained from 3 conscious dogs, provided with a chronic gastric fistula. Outputs of acid (mequiv min?1) and PGs (pg min?1) were measured in gastric secretions stimulated by pentagastrin (100 or 200 ng kg?1min?1). Prostaglandin activity was estimated, after extraction and thin layer chromatography, by radioimmuno-assay of the PGB formed by treatment with alkali. Tritiated PGs were added to gastric juice for the purpose of correcting for PGs recovery. Using this method, the minimum mass of PGB which could be satisfactorily distinguished from zero was 25 pg. Prostaglandins A2 and E2 were present in pentagastrin-activated gastric secretions and averaged (mean ± SE, n = 8) 200.7 ± 18.1 and 260.1 ± 18.0 pg min?1 respectively. The identity of PGA2 and PGE2 was confirmed by gas liquid chromatography combined with mass spectrometry. The amount of PGE2 converted to PGA2 during extraction, separation and conversion procedures was estimated from the amount of [3H] PGA2 found when only [3H] PGE2 had been added to a sample of gastric juice and averaged 14.5% ± 2.0. Our preliminary results support the possibility that PGE2 and PGA2 may be of physiological importance in the regulation of canine gastric secretions.  相似文献   

6.
Pretreatment of human lung fibroblasts with PGE2 but not PGF enhanced synthesis of prostaglandins (PGs). The effect of the pretreatment on PG synthesis was related to the concentration of PGE2 that was added to the culture medium. Pretreatment with PGE2 at 5 × 10−12M did not enhance PG synthesis whereas pretreatment with PGE2 at 5 × 10−6M induced a maximal effect. Production of PGs was increased following 1 day of pretreatment with PGE2 and was increased further following 3 days of pretreatment. The PGE2 treated cells showed only a slight increase in the bradykinin-induced release of radioactivity from cells prelabeled with [3H]arachidonic acid but showed a dramatic increase in the bradykinin-induced synthesis of radio-labeled PGs. The conversion of free arachidonate to PGs in both intact cells and in a cell-free preparation was increased by PGE2 pretreatment. The presence of cyclohexamide during the pretreatment did not inhibit the PGE2-induced activation of PG synthesis. Taken together, the results indicate that pretreatment of cells with PGE2 increased PG synthesis by augmenting the conversion of arachidonate to PGs.  相似文献   

7.
Gastrotoxic activities of different non-steroidal anti-inflammatory drugs (NSAIDs) (diclofenac, indomethacin, ketoprofen, naproxen and piroxicam) administered per os were compared with their ability to inhibit gastric prostaglandin E2 (PGE2) synthesis in the rat. In a parallel study, effects of pretreatment with zinc acexamate (ZAC) were also assessed. NSAIDs invariably caused gastric mucosal damage and a decrease of PGE2 levels. A good correlation between the decrease of PGE2 levels and the index of gastric lesion (r = 0.41; p < 0.021) was observed when results obtained with the different NSAIDs were pooled. ZAC pretreatment significantly decreased the overall severity of lesions induced by NSAIDs. However, no correlation between gastric lesion index and depletion of PGE2 gastric levels was observed after treatment with ZAC (r = 0.012; p < 0.948). These data corroborate the hypothesis that preservation of the capability to synthesize endogenous PGs is of critical importance in the maintenance of gastric mucosal integrity. The gastroprotective action observed with ZAC involves alternative mechanisms other than modification of PGE2 levels.  相似文献   

8.
The compound 7-OPyA has been reported to antagonize smooth muscle stimulatory effects of some protaglandins (PG's) in vitro. The in vivo PG antagonists activity of 7-OPyA was reported to antagonize PGE-induced diarrhea in mice. We studied the effects of this compound on PGE1 induced inhibition of gastric secretion in unanesthetized dogs. Secretion was stimulated by continuous intravenous infusion of histamine. At the steady-state plateau of gastric secretion, PGE1 methyl ester (PGE1 ME) or PGE1 ME and 7-OPyA were simultaneously infused intravenously. The extent of gastric secretory inhibition afforded by PGE1 ME alone or in the presence of 7-OPyA was assessed. 7-OPyA did not modify PGE1 ME gastric antisecretory actions when administered at doses 20–50 times greater than the dose of PGE1 ME. These results suggest that the prostaglandin antagonist effects of 7-OPyA show organ specificity, which may be of clinical importance.  相似文献   

9.
To determine the influence of prostaglandins on cAMP metabolism in renal papillary collecting tubule (RPCT) cells, intracellular cAMP levels were measured after incubating cells with prostaglandins (PGs) alone or in combination with arginine vasopressin (AVP). PGE1, PGE2 and PGI2, but not PGD2 or PGF, increased intracellular cAMP concentrations. At maximal concentrations (10−5 tthe effects of PGE2 plus PGI2 (or PGE1), but not of PGI2 plus PGE1, were additive suggesting that at least two different PG receptors may be present in RPCT cell populations. Bradykinin treatment of RPCT cells caused an accumulation of intracellular cAMP which was blocked by aspirin and was quantitatively similar to that observed with 10−5 PGE2. PGs, when tested at concentrations (e.g. 10−9 ) which had no independent effect on intracellular cAMP levels, did not inhibit the AVP-induced accumulation of intracellular cAMP in RPCT cells. These results indicate that PGs do not block AVP-induced accumulation of intracellular cAMP in RPCT cells at concentrations of PGs which have been shown to inhibit the hydroosmatic effect of AVP on perfused collecting tubule segments. However, at higher concentrations of PGs (e.g. 10−5 ), the effects of AVP plus PGE1, PGE2, PGI2 or bradykinin on intracellular cAMP levels were not additive. Thus, under certain conditions, there is an interaction between PGs and AVP at the level of cAMP metabolism in RPCT cells.  相似文献   

10.
Experiments were carried out to assess the influence of prostaglandins (viz. PGE1, PGE2 and PGF) on plasma concentrations of FSH and LH in the female rhesus monkey. Monkeys were ovariectomized and treated with estradiol benzoate to suppress endogenous gonadotropin levels prior to these experiments. Femoral venous blood was taken at intervals following a single carotid arterial injection of the PG in anesthetized monkeys. FSH and LH concentrations, determined by radioimmunoassay, were not significantly altered in 4 control animals receiving saline (2) or ethanol-saline (2), the vehicles for PGF and for the E series PGs, respectively. PGE1 (5mg) effected dramatic elevations of LH within 5 min in 3 animals and the high plasma concentrations were maintained at least for 60 min. Similarly, 5.0 mg of PGE2 effected rapid elevation of LH concentrations, from 2- to 7-fold pre-injection levels in 3 animals. In contrast, FSH levels were not so markedly altered by PGE1 and PGE2, but in general, appeared to be somewhat decreased by these treatments. PGF had no effect on plasma FSH and LH concentrations. These data demonstrate the ability of PGs of the E series to elevate plasma LH concentrations in the rhesus monkey and support studies in other species suggesting a modulating role for PGs on gonadotropin secretion or release.  相似文献   

11.
Gastroprotection associated with the intragastric administration of prostaglandin (PG) precursor fatty acids such as linoleic (LA), gamma-linolenic (GLA), and arachidionic acid (AA) has been reported to be mediated via their conversion to PGs. This report examines the relationship between gastroprotection and the extent/rate of PG-release in rats intragastrically administered PG biosynthetic precursors: LA, AA, dihomo-gamma-linolenic acid (DHGL) or oleic acid (OA, a nonprecursor fatty acid). At various times following intragastic administration of a fatty acid, gastric fluid was collected, extracted, chromatographed, and assayed for PGE1 or PGE2 by specific radioimmunoassay. AA and DHGL dose dependently elevated gastric PGE2 and PGE1 levels, respectively. Maximal PGE elevation, 200–400 ng/stomach, was over 400-fold above basal values, and observed within 5–10 minutes of administration. Conversely, OA and LA elicited only a minor (2–10 fold) stimulation of PGE release. In contrast to effects on PG release, all four fatty acids protected the gastric mucosa against macroscopic damage induced by ethanol. The apparent rank order of potency was AA > DHGL = LA > OA (the difference in potency between DHGL or LA and OA was not significant). Since LA and OA (a nonprecursor) only marginally elevated lumenal PGs relative to DHGL or AA, yet were equally efficacious in the gastroprotection assay, it is likely the other fatty acid-related mechanisms play an important role in protecting the stomach against ethanol-induced injury.  相似文献   

12.
13.
Effects of parathyroid hormone (PTH) and several prostaglandins (PGs) on cyclic AMP (cAMP) metabolism were studied and compared in isolated renal cortical tubules from male hamsters. Both production and intracellular degradation of cAMP were increased by PTH and each of the PGs tested (PGE2, PGE1, PGI2). Production of cAMP was increased to similar levels by maximal concentrations of PTH and each PG, however, degradation of cAMP was significantly higher in response to PTH than with any of the PGs. This difference in intracellular degradation of cAMP was responsible for the much higher concentrations of cAMP in renal cortical tubules exposed to PGs (PGE1, PGE2, PGI2) than to PTH. Submaximal amounts of each PG produced additive increases in cAMP concentrations in the presence of maximal amounts of PTH. Additivity of the combined responses was lost, however, as the PGs concentrations reached their maximas. The results suggest that renal PGs (PGE2 and PGI2) may modulate the effects of PTH on cAMP concentrations in renal cortical tubules.  相似文献   

14.
Prostaglandins (PGs) are signaling lipids derived from arachidonic acid (AA), which is metabolized by cyclooxygenase (COX)-1 or 2 and class-specific synthases to generate PGD2, PGE2, PGF, PGI2 (prostacyclin), and thromboxane A2. PGs signal through G-protein coupled receptors (GPCRs) and are important modulators of an array of physiological functions, including systemic inflammation and insulin secretion from pancreatic islets. The role of PGs in β-cell function has been an active area of interest, beginning in the 1970s. Early studies demonstrated that PGE2 inhibits glucose-stimulated insulin secretion (GSIS), although more recent studies have questioned this inhibitory action of PGE2. The PGE2 receptor EP3 and one of the G-proteins that couples to EP3, GαZ, have been identified as negative regulators of β-cell proliferation and survival. Conversely, PGI2 and its receptor, IP, play a positive role in the β-cell by enhancing GSIS and preserving β-cell mass in response to the β-cell toxin streptozotocin (STZ). In comparison to PGE2 and PGI2, little is known about the function of the remaining PGs within islets. In this review, we discuss the roles of PGs, particularly PGE2 and PGI2, PG receptors, and downstream signaling events that alter β-cell function and regulation of β-cell mass.  相似文献   

15.
In the perfused mesenteric artery of the rat prostaglandins (PGs) E1, E2 and I2 had distinct actions. PGE2 potentiated pressor responses to noradrenaline, angiotensin II and potassium ions. PGE1 potentiated responses to noradrenaline and angiotensin at low concentrations and inhibited them at high concentrations: no concentrations had any effect on potassium responses. PGI2 inhibited responses to noradrenaline and angiotensin but had no effect on potassium responses. These three distinct actions suggest that the binding sites for the three PGs in this vascular muscle must be distinct.  相似文献   

16.
Prostaglandins (PG)I2, PGE2 and 6-keto PGF1α were infused directly into the gastric arterial supply at 10−9, 10−8 and 10−7 g/kg/min during an intra-gastric artery pentagastrin infusion in anesthetized dogs. 6-keto PGF1α was also infused at 10−6 g/kg/min. Gastric arterial blood flow was measured continuously with a non-cannulating electromagnetic flow probe and gastric acid collected directly from the stomach. PGI2 and PGE2 produced similar dose-dependent increases in blood flow with an increase of more than four-fold at the highest dose. Both PGs inhibited acid output over this dose range with PGE2 having 10 times the potency of PGI2. 6-keto PGF1α was at least 1000 times less active than PGI2 or PGE2 at increasing blood flow and failed to inhibit acid output even at 10−6 g/kg/min.  相似文献   

17.
In the past two decades there have been innumerable reports that prostaglandins (PGs) are essential for mammalian ovulation. However, we have recently found that a relatively low dose of 0.03 mg indomethacin (INDO) sc to PMSG/hCG-primed immature Wistar rats can significantly reduce ovarian PG levels without inhibiting the control ovulation rate of 60+ ova/rat (1–3). In view of this information, the present study was an effort to duplicate the earlier reports that PGs can reverse the “inhibitory” effect of INDO on ovulation. In control animals, which received PMSG and hCG only, the ovulation rate was 63.8 ± 4.5 ova/rat. This rate was reduced to 4.1 ± 1.1 ova/rat when the animals were injected with 1.0 mg INDO at 3 h after hCG. In no instance was this inhibition reversed when the animals were treated with 1.0 mg of PGE2 or PGF2α, or a combination of both prostanoids in either a single dose at 3 h after hCG, or in 4× doses at 2-h intervals beginning at 3 h after hCG. Furthermore, in animals that did not receive INDO, the ovulation rate in PGE2-treated animals was reduced to 20.0 ± 6.7 ova/rat, and in animals treated with PGE2 and PGF2α (combined) it was reduced to 19.4 ± 6.5 ova/rat. In summary, not only did the PGs fail to reverse the anti-ovulatory effect of INDO, PGE2 actually suppressed the ovulation rate.  相似文献   

18.
19.
The ability of various prostaglandins (PGs) to affect the anamnestic immune response of keyhole limpet hemocyanin (KLH)-primed rabbit popliteal lymph node cells was investigated. Of the four PGs studied (PGA1, PGE2 and PGF), PGE1 was found to have a stimulatory effect, whereas PGA1, PGE2 and PGF were ineffective in stimulating or inhibiting the anamnestic response. Under the conditions studied, a 3.5-fold increase in antibody production was obtained in PGE1-treated, KLH-stimulated cultures. Maximum enhancement was obtained when 0.2 μg of PGE1 were added at the time of culture initiation and were allowed to remain in contact with the lymph node cells for 24 hours.  相似文献   

20.
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