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1.
The ability of 8-ethoxycarbonyl-10, 11 dihydro-A-prostaglandin(HR 546) to antagonise smooth muscle contracting effect of prostaglandins E2 and F on isolated preparations of rat and hamster stomach fundus, guinea pig ileum and gerbil colon has been studied. HR 546 was found to be a potent, non-specific, probably competitive, prostaglandin antagonis on these four smooth muscle preparations.  相似文献   

2.
The synthesis of 2-decarboxy-2-(tetrazol-5-yl)prostaglandins of the E1, E2, F1α and F2α series is described together with their biological effects on gerbil colon smooth muscle and rat blood pressure.  相似文献   

3.
The synthesis of 2-decarboxy-2-(tetrazol-5-yl)prostaglandins of the E1, E2, F1α and F2α series is described together with their biological effects on gerbil colon smooth muscle and rat blood pressure.  相似文献   

4.
Whole cell preparations of rat stomach corpus, jejunum, and colon were incubated and the released prostaglandin E2 (PGE2), PGF, PGD2, 15 keto-13,14 dihydro PGE2, and 15 keto-13,14 dihydro PGF were measured by combined gas chromatography-mass spectrometry. All regions made PGD2 and possessed a high capacity for producing 15 keto-13,14 dihydro derivatives of both PGE2 and PGF. Hypertonic sucrose solutions resulted in concentration-dependent increases in prostaglandin release, particularly of PGE2 and its metabolite. It is suggested that PG's may play a role in the local effects of luminal hyperosomolarity on digestive tract functions.  相似文献   

5.
The effects of prostaglandins A2, A1, F, E2, E1, F and an analog of PGH2 upon calcium release from mitochondria isolated from bovine intrapulmonary vein and contraction of helical strips of the same tissue were determined. The order of activity of the prostaglandins for calcium release was similar to that for contraction with the exception of the PGH2 analog. It is suggested that prostaglandin A2, F, E2 and A1 induced release of mitochondrial calcium may influence the contractile state of bovine intrapulmonary vein. However, the PGH2 analog has a subcellular mechanism other than or in addition to mitochondrial calcium release and is different from the other prostaglandins.  相似文献   

6.
Effects of prostaglandins (PGs) E1, E2, F and I2 in a wide range of concentration were examined in mesenteric and cerebral arteries isolated from mature baboons. PGs E1, E2 and F at low concentrations (10−10 to 10−7 M) elicited relaxation in helically cut strips of cerebral arteries precontracted with phenylephrine. In contrast, the PGs did not cause relaxation in the mesentric artery. PGI2 (10−9 to 10−6 M) produced marked relaxation in both arteries. The EC25 for PGI2 in the mesenteric artery was significantly lower than that in the cerebral artery. During baseline conditions, cerebral arteries contracted in response to high concentrations (greater than 10−7 M) of PGs E1, E2 and F. In mesentric arteries, a large contraction was induced by PGs F and E2 but not by PGE1. Arachidonic acid (10−6 M) produced an aspirin-inhibitable relaxation in both arteries to a similar extent, so that the vasodilator PG(s) formed in the two different arterial walls appear to exert a similar relaxant action. Thus, the baboon mesenteric artery was more sensitive to PGI2 for the relaxant effect than was the cerebral artery, while PGs F, E1 and E2 caused only a contraction in the mesenteric artery but both relaxation and contraction in the cerebral artery.  相似文献   

7.
The relative potencies of the prostaglandins A1, A2, E1, E2, F and their 15-keto-, 15-keto-13,14-dihydro-, and 13,14-dihydro-metabolites were investigated on isolated lamb ductus arteriosus preparations contracted by exposure to elevated PO2. All the prostaglandins (except PGF and its 15-keto-metabolites) relaxed the tissue. However, only PGE1, E2, and their 13,14-dihydro-metabolites, were effective at concentrations below 10−8 M. Therefore, events that alter metabolism of circulating PGs in the perinatal period may have significant effects on the relative patency or closure of the ductus arteriosus.  相似文献   

8.
Radioimmunoassays of platelet prostaglandins E1 and F in platelet rich plasma or platelet suspension, demonstrate that both PGE1 and PGF are present at higher concentrations than prostaglandins E2 and F. Gas chromatography — mass spectrometry determinations of prostaglandins E1 and E2 in resting washed platelets confirm this difference. Lastly, there is a greater incorporation of [1-14C] acetate into prostaglandins E1 and F compared to that into prostaglandins E2 and F.  相似文献   

9.
Bovine gastric mucosal and muscle microsomes synthesize prostaglandins and thromboxane B2 (TXB2) from arachidonic acid (AA). TXB2 and 6-keto-prostaglandin F1α (6-keto-PGF1α) were the major products synthesized by pylorus, body, and cardiac region of the gastric mucosa. Gastric muscle mainly synthesized 6-keto-PGF1α. TXB2 and 6-keto-PGF1α synthesis occurs at an appreciable rate from endogenous precursors but more rapidly with added arachidonate. Prostaglandins E2, F2α and D2 were synthesized in smaller amounts under the conditions studied.  相似文献   

10.
Blood pressure and heart rate effects of prostaglandin E2 and F were examines after administrating each agent into the left lateral brain ventricle of chloralose-anesthethized cats. Administration of prostaglandin E2 (1 μg) resulted in significant, prolonged increases in arterial pressure (25.7 ± 6.7 mm Hg) and heart rate (19.4 ± 7.7 beats/min). These responses were mimicked when the same dose of prostagland E2 was administered into the restricted to the lateral and third ventricles via cannulation of the cerebral aqueduct, whereas no significant cardiovascular occured with administration into the fourth ventricle. Intravenous injection of prostaglandin E2 resulted in a transient decrease in blood pressure but no change in heart rate. Administration of prostaglandin F (1 and 3 μg) into the CNS produced no significant cardiovascular responses. The same was true when prostaglandin F was administered by the intravenous route. These results indicate that pronounced cardiovascular effects can be produced by administering prostaglandin E2 but not F into the CNSm and that the central site of action of prostaglandin E2 is in the forebrain.  相似文献   

11.
Spontaneous changes in isometric developed tension (IDT) as a function of time after isolation (contractile constancy) in uteri from control-castrated and castrated chronic streptozotocin-diabetic rats, were explored. The effects of injecting 17-beta estradiol (E0) were also studied. No differences in the minor changes of contractile constancy, between control and diabetic preparations, during a period of 60 min, were detected, whereas uteri from non-diabetic EO injected animals (0.5+1.0 ug, prior to sacrifice), exhibited a profound reduction of IDT, significantly greater than in tissues obtained from E0 injected-diabetic rats. Moreover, basal generation and outputs into the suspending solution of prostaglandins (PGs) E1, E2 and F, were explored in the same groups, at 60 min following tissue isolation. The basal outputs of these three PGs were similar in castrated control rats, but preparations from castrated-diabetics released significantly more PGE1. The administration of E0 to castrated-diabetics, failed to alter the releases of the three PGs explored. In addition, the metabolism of labelled arachidonic acid (AA) into different prostanoids (6-keto-PGF1, PGF2, PGE2 and thromboxane B2-TXB2), was also investigated. The non-diabetic spayed rat uterus converted AA into these four prostanoids, the transformation into 6-keto-PGF1α (as an index of PGI2 formation) being the most prominent. In preparations from diabetic rats the formation) being the most prominent. In preparations from diabetic rats the formation of 6-keto-PGF1α, PGF2α and PGE2, was significantly smaller than in controls, whereas a greater % of TXB2 formation (as an index of TXA2), was detected. On the other hand uterine preparations from non-diabetic spayed rats injected with E0 formed less 6-
amounts of PGF2α or of TXB2 from AA, than E0 injected controls, whereas uteri from castrated diabetic animals injected with E0, formed a similar % of 6-keto-PGF1α, PGF2α and PGE2 from AA, than tissue preparations from non-estrogenized controls. However, the enhanced transformation of the labelled fatty acid precursor (AA) into TXB2 in the diabetic group, was significantly reduced by the steroid. The role of the augmented generation and release of PGE1 in uteri from diabetic rats is discussed in terms of precedents indicating the relevance of PGs type E supporting rat uterine motility. In addition the influence of E0 is attractive, because its reducing effect on TX production, in diabetes, a disease known to be accompanied by enhanced synthesis of vasoconstrictor and platelet aggregation TXA2, and by frequent obstructive circulatory problems.  相似文献   

12.
The release of prostaglandin E2 and F, thromboxane B2 and 6-keto-prostaglandin F was measured in isolated human placental cotyledons perfused under high- and low-oxygen conditions. Also the effect of reoxygenation on prostaglandin production was studied. During the high-oxygen period, prostaglandin E2 accounted for 44 % and 6-keto-prostaglandin F for 28 % of all prostaglandin release, and the rank order of prostaglandin release was E2 > 6-keto-prostaglandin F > thromboxane B2 > prostaglandin F. Hypoxia had no significant effect on quantitative prostaglandin release, but the ration of prostaglandin E2 to prostaglandin F was significantly increased. After the hypoxic period during reoxygenation the release of 6-keto-prostaglandin F was significantly decreased, as was the ratio of 6-keto-prostaglandin F to thromboxane B2. Also the ratio of the vasodilating prostaglandins (E2, 6-keto-prostaglandin F) to the vasocontricting prostaglandins (thromboxane B2, prostaglandin F) was decreased during reoxygenation period. With the constant flow rate, the perfusion pressure increased during hypoxia in six and was unchanged in three preparation. The results indicate that changes in the tissue oxygenation in the placenta affect prostaglandin release in the fetal placental circulation. This may also have circulatory consequences.  相似文献   

13.
The effect of six naturally occurring prostaglandins on isolated umbilical arteries and veins has been studied. All six prostaglandins had a constricting effect on the umbilical vessels. On the umbilical artery preparations the potencies in decreasing order were A2>B2>F>B1>E2>A1. Prostaglandin B2 was more potent than PGA2 on the umbilical vein. Polyphloretin phosphate (PPP) antagonised the constricting effect of all six prostaglandins without altering responses to 5-hydroxytryptamine.  相似文献   

14.
11-Deoxy-16,16-trimethyleneprostaglandin E1 is a potent inhibitor of prostaglandin E-induced contractions of the gerbil colon. The antagonism is directed specifically against the prostaglandin E receptor and is not manifested when contractions are induced by either prostaglandin F or acetylcholine.  相似文献   

15.
Prostaglandins may be implicated in the bronchoconstriction which occurs in asthma. Prostaglandins F (PGF and D2 (PGD2) have been reported to produce bronchoconstriction in asthmatic subjects in vivo and PGF cotnracts human isolated airway smooth muscle. We examined the relative efficacy and potency of PGF and PGD2 on human bronchial spiral strips taken from 6 patients at thoracotomy. PGF had greater efficacy than PGD2. The mean % Tmax (percentage of maximal contractile response) ± s.e. mean were 84 ± 7 and 54 ±7 respectively (P < 0.05). PGF (mean pD2 ± s.e. mean = 6.39 ± 0.6) tended to be more potent than PGD2 (5.68 ± 0.2). Since, in vivo, PGD2 has greater efficacy and potency than PGF, our results suggest that the in vivo effect of these prostaglandins does not result solely from an action on airway muscle.  相似文献   

16.
In the anesthetised dog an infusion of exogenous prostaglandin E1 (100μG/min) inhibits the pulmonary vascular pressor response to hypoxia. Both 25 and 100 μG/min PGE1 can reduce the transient pulmonary hypertension caused by a bolus of prostaglandin F. This suggests that hypoxia and PGF2α may share a final common pathway in producing pulmonary vasoconstriction. These results may help to explain the mechanism by which endotoxin inhibits the pulmonary vascular response to hypoxia. This effect is probably achieved by stimulating the production of an endogenous dilator prostaglandin. Exogenous PGE1 can mimic this effect.  相似文献   

17.
An original perifusion device which allows a discrimination between the 30 mn releases of prostaglandins F2α and E2 by the luminal and the myometrial faces of sheep endometrium is described. Tissue was sampled on day 4, 14, 16 or 17 of the cycle and on day 14 or 17 of pregnancy. Total prostaglandin (PG) release measured with this device was in good agreement with PG's concentrations in media of in vitro endometrium incubations already described.Discrimination analysis of the PGs release by each side of the endometrial tissue during the 30 mn perifusion time releaved that PGF2α concentrations of the perifusion medium issued from the lumen compartment were higher than those of the myometrial compartment in all physiological status where corpus luteum is active (including early pregnancy). Therefore in the ewe, it seems that luteal structure maintenance during early pregnancy is not due, as in the giltm to a shift in PGF2α secretion towards the uterine lumen.  相似文献   

18.
The role of the central nervous system (CNS) in the antiarrhythmic effects of prostaglandins (PGs) E2, F, and I2 was studied by administering each agent into the left lateral cerebral ventricle (i.c.v. administration) of chloralose-anesthetized cats. The cardiac arrhythmias were produced by intravenous (i.v.) infusion of ouabain (1 μg/kg/min). The PGs E2, F and I2 on i.c.v. administration in the dose range of 1 ng to 10 μg failed to inhibit ouabain-induced cardiac arrhythmias. However, when infused i.v., PGE2 (1 μg/kg/min), PGF (5 μg/kg/min), and PGI2 (2 μg/kg/min) effectively suppressed these arrhythmias. The standard antiarrhythmic drug propanolol (0.5–8.0 mg)oni.c.v.administration also significantly reduced the ouabain-induced cardiac arrhythmias. It is suggested that the CNS is not the site of action of PGs E2, F, and I2 in antagonising the ouabain-induced cardiotoxicity in cats.  相似文献   

19.
This study establishes some correlations between molecular structure and surface function of six prostaglandins in a model membrane system. Using spread films at the air/water interface, we determined surface pressure and surface potential of PGs A1, A2, E1, E2, F and F. All the PGs formed films with low pressure (0 to 9 dyne/cm) and relatively low surface potentials (ΔV = 10 to 250 mV). On 0.15 M NaCl, the π and ΔV values were in the order E1 > F > A1 > F > A1 > F2α = A2 > E2 and F > E1 > A1 > A2 > F > E2 respectively. Clearly, the cis unsaturation in the carboxylic chain of the PG2 series conferred greater instability to the films, as indicated by the lowest π and ΔV values. Also, members of the PG1 series penetrated films of dipalmitoyl phosphatidyl choline (DPPC) better than PG2 did, the ablest being E1 (Δπ = 12 dyne/cm) and the poorest F2α (Δπ = 2 dyne/cm); penetration of E1 and F2α was independent of the initial pressure (πi) of the DPPC film, whereas with A1 and F Δπ decreased as πi increased. The PGs expressed marked discriminating capacities for the electrolyte, as indicated by differences in their π and ΔV responses to Na+ and Ca++ as well as for the lipid, as indicated by different penetration (Δπ values) into DPPC films.  相似文献   

20.

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 F(PGF) 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 PGF-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 PGF-and PGE2-release from tracheal rings was significantly reduced by U-0126 and indomethacin, but not by Y-27632. Also, PGF-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   

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