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1.
The interaction of prostaglandin E2 (PGE2) and aspirin with the responses to peri-arterial stimulation (PS) and norepinephrine (NE) was studied in the isolated kidney of rabbit perfused through the renal artery at constant flow with Krebs' solution. NE and PS increased vascular perfusion pressure of kidney and caused a contraction on the isolated rabbit aortic strip superfused with the effluent from kidney. Addition of PGE2 to the perfusion medium decreased the PS-induced rise in perfusion pressure without changing the effect of exogenous NE. In contrast, addition of aspirin to the perfusion medium induced a potentiation of the response to PS but not to NE. These results suggest that PGE2 modulates the effect of PS probably by inhibiting the release of NE from sympathetic nerve endings. 相似文献
2.
Summary The effect of quinidine on Na and H+ transport by the turtle bladder and water transport by the toad bladder was examined. Quinidine inhibited the short-circuit current and the potential difference in a dose-dependent fashion. The effect of quinidine on the short-circuit was not dependent on extracellular calcium concentration and was not reversible with removal of the drug. Quinidine inhibited H+ secretion in a dose-dependent fashion. The effect of quinidine on H+ secretion also was not dependent on extracellular calcium concentration and was not reversible, either with removal of the drug or with stimulation of H+ secretion with 5% CO2. The effect of quinidine on Na or H+ transport could not be elicited by an equivalent dose of tetracaine, suggesting that the inhibitory effect of quinidine is not dependent on its anesthetic properties. Quinidine also inhibited vasopressin and cyclic AMP stimulated water flow in the toad bladder. Quinidine did not alter calcium uptake by the turtle bladder but increased calcium efflux by the turtle and toad bladders. These observations suggest that a rise in cytosolic calcium is responsible for the inhibitory effect of quinidine on Na, H+, and water transport. 相似文献
3.
Effect of prostaglandin E2 on vascular responses of the rabbit kidney to nerve stimulation and noradrenaline, in vitro and in situ 总被引:2,自引:0,他引:2
The effect of prostaglandin E2 on vascular responses of the rabbit kidney to renal nerve stimulation and noradrenaline was examined and as a test of the hypthesis that prostaglandins of the E series may be involved in the regulation of adrenergic neuroeffector transmission. Intraarterial administration of prostaglandin E2 to the kidney caused marked inhibition of vascular responses to nerve stimulation whereas the responses to noradrenaline were not significantly altered. In the preparation, vascular responses to both nerve stimulation and noradrenaline were inhibited by prostaglandin E2 infusion, although its effect on responses to nerve stimulation was approximately twice that observed on responses to noradrenaline.It is concluded that prostaglandin E2 acts primarily at a prejunctional level of adrenergic neuroeffector transmission in the kidney, although a postjunctional effect has also been observed. 相似文献
4.
The effects of orally administered prostaglandin E2, 16,16-dimethyl prostaglandin E2 and U-46619, an analogue of the prostaglandin endoperoxide PGH2, on gastric secretory volume, acid and mucus were studied in the rat. All of the compounds significantly increased the volume of gastric secretion, mucus secretion, measured as N-acetylneuraminic acid and mucus synthesis measured as the incorporation of [3H]-glucosamine into mucosal glycoprotein; however, only PGE2 and 16,16-dimethyl PGE2 inhibited acid secretion. U-46619, 1.5 mg/kg provided significant protection against ethanol-induced gastric ulcers, an effect that has been previously shown for the other two compounds. These studies provide additional evidence that prostaglandin induced mucosal protection may by related to an effect on mucus and on stimulation of nonparietal cell gastric secretion. Further study of these parameters may be important in the development of antiulcer drugs for long term clinical use. 相似文献
5.
Jiri Turinsky Daniel J. Loegering 《Biochimica et Biophysica Acta (BBA)/General Subjects》1985,840(1):137-140
Rats were injected intraperitoneally withPseudomonas aeruginosa (septic group) or sterile 0.9% NaCl (controls). Soleus muscles were excised 7 h later, and muscle prostaglandin E2 release and tyrosine release were measured in vitro. Muscles of septic rats exhibited 226–326% higher release of prostaglandin E2 and 54–84% higher net proteolysis than muscles of controls. Inclusion of aspirin or indomethacin in the incubation medium almost completely inhibited prostaglandin E2 production, but had no effect on net proteolysis in muscles from either group. Inclusion of cycloheximide, a protein synthesis inhibitor, increased tyrosine release of control muscles by 42%, whereas no statistically significant increase was observed in muscles from infected rats. However, total proteolytic rate, indexed by tyrosine release in the presence of cycloheximide, was 22% higher in muscles of septic rats compared to that of control animals. Concomitantly, inclusion of cycloheximide inhibited prostaglandin E2 release by muscles of infected rats by 91% and that of controls by 65%. It is concluded that (a) muscles of septic animals exhibit a pronounced stimulation of prostaglandin E2 release and net proteolysis, combined with a small increase in total proteolytic rate, (b) the stimulation of net proteolysis is mainly due to inhibition of protein synthesis, (c) the increases in net and total proteolysis appear to be independent of prostaglandin E2 production, (d) cycloheximide has a previously unrecognized inhibitory effect on muscle prostaglandin E2 production. 相似文献
6.
J.L. Black P.R.A. Johnson M. Alfredson C.L. Armour 《Prostaglandins & other lipid mediators》1989,37(3)
Prostaglandins have been implicated in the development of airway hyperresponsiveness, and this may be mediated via modulation of neurotransmission. We compared the effects of prostaglandin E2 on the contractile response to electrical field stimulation in rabbit and human bronchus. Prostaglandin E2 produced marked inhibition in rabbit bronchus (mean % inhibition 35±17, P< 0.05) but was without effect in human bronchus. The inhibition in rabbit bronchus was not the result of a direct effect on muscle tone and the site of action is likely to be pre-synaptic since prostaglandin E2 had only minor effects on exogenous acetylcholine. Since prostaglandins are known to affect calcium mobilization, we compared the dependence of cholinergic stimulation on the calcium voltage dependent channel (VDC) in the two species. Cholinergic stimulation was dependent on the VDC in rabbit but not human bronchus and this may be an explanation for the different effects of prostaglandin E2 in the two species. 相似文献
7.
Leonard C. Best Elisabeth A. Bone Peter B.B. Jones R. Graham G. Russell 《Biochimica et Biophysica Acta (BBA)/General Subjects》1980,632(2):336-342
La3+ was found to inhibit the secretion of 5-hydroxytryptamine and the production of thromboxane B2 by washed platelets exposed to collagen or thrombin. In addition, La3+ inhibited secretion in response to sodium arachidonate, although the conversion of arachidonate to thromboxane B2 was not affected.La3+ was also found to enhance the accumulation of cyclic AMP under basal conditions and in response to prostaglandin E1, in washed platelets. The inhibition of cyclic AMP accumulation by ADP was prevented by La3+, suggesting that the effect of ADP on cyclic AMP metabolism was dependent upon the presence or flux of calcium at the platelet membrane.La3+ inhibited the activity of adenylate cyclase in platelet lysates both in response to prostaglandin E1 and to F?, indicating a possible effect at the catalytic subunit of the enzyme. None of the observed effects of La3+ could be reversed by the addition of Ca2+ up to 10 mM. The stimulation of cyclic AMP production by La3+ may largely explain the inhibitory effect of La3+ upon platelet secretion and thromboxane B2 production. These results also suggest that Ca2+ localised at the platelet plasma membrane may be important in the regulation of cyclic AMP metabolism. 相似文献
8.
《Prostaglandins and medicine》1979,2(4):285-291
Small intestinal fluid secretion induced by oral prostaglandin E2 in fasted rats was analyzed for various ionic components. Rat intestinal fluid had elevated calcium and potassium as well as decreased sodium and chloride concentrations relative to plasma electrolytes. Either low dose prostaglandin (0.15 mg/kg) or 1 ml of intragastric mannitol (5%) induced accumulation in the small intestine of fluid that had elevated chloride and depressed calcium and sodium concentrations compared to vehicle-treated controls. Higher doses of prostaglandin (1.0 mg/kg) led to secretions with increased sodium and chloride concentrations with respect to mannitol-induced fluid. Electrolyte concentrations in fluid induced by low dose prostaglandin appear to be similar to those in fluid caused by osmotically-induced changes. Higher doses of prostaglandin E2 induce additional electrolyte alterations which may result from modified gut transport of water and ions. 相似文献
9.
Bie Shung Tsai Robert J. Lefkowitz 《Biochimica et Biophysica Acta (BBA)/General Subjects》1979,587(1):28-41
We report that the adenylate cyclase system in human platelets is subject to multiple regulation by guanine nucleotides. Previously it has been reported that GTP is either required for or has little effect on the response of the enzyme to prostaglandin E1. We have found that when platelet lysates were prepared in the presence of 5 mM EDTA, GTP lowered the basal and prostaglandin E1-stimulated adenylate cyclase activity when the enzyme was assayed in the presence of Mg2+. The basal and prostaglandin E1-stimulated adenylate cyclase activities were also increased by washing, which presumably removes endogenous GTP. The analog, guanyl-5′-yl-imidodiphosphate mimics the inhibitory effect of GTP on prostaglandin E1-stimulated adenylate cyclase activity but it stimulates basal enzyme activity. The onset of the inhibitory effect of GTP on the adenylate cyclase system is rapid (1 min) and is maintained at a constant rate during incubation for 10 min. GTP and guanyl-5′-yl-imidodiphosphate were noncompetitive inhibitors of prostaglandin E1. An increase in the concentration of Mg2+ gradually reduces the effect of GTP while having little influence on the effect of guanyl-5′-yl-imidodiphosphate. Neither the substrate concentration nor the pH (7.2–8.5) is related to the inhibitory effect of guanine nucleotides. The inhibition by nucleotides was found to show a specificity for purine nucleotides with the order of potency being guanyl-5′-yl-imidodiphosphate > dGTP > GTP > ITP > XTP > CTP > TTP. The inhibitory effect of GTP is reversible while the effect of guanyl-5′-yl-imidodiphosphate is irreversible. The GTP inhibitory effect was abolished by preparing the lysates in the presence of Ca2+. However, the inhibitory effect of guanyl-5′-yl-imidodiphosphate persisted. Substitution of Mn2+ for Mg2+ in the assay medium resulted in a diminution of the inhibitory effect of GTP on basal activity and converted the inhibitory effect of GTP on prostaglandin E1-stimulated activity to a stimulatory effect. At a lower concentration of Mn2+ (less than 2 mM) guanyl-5′-yl-imidodiphosphate inhibited prostaglandin E1-stimulated adenylate cyclase activity, but at a higher concentration of Mn2+, it caused an increase in enzyme activity exceeding that occuring in the presence of prostaglandin E1. In the presence of Mn2+, dGTP mimics the effect of GTP and is 50% as effective as GTP. Our data suggest that the inhibitory effect of GTP on prostaglandin E1-stimulated adenylate cyclase is mainly due to its direct effect on the enzyme itself, whereas the stimulatory effect of GTP on prostaglandin E1-stimulated adenylate cyclase is due to enhancement of the coupling between the prostaglandin E1 receptor and adenylate cyclase. These studies also indicate that the method of preparation of platelet lysates can profoundly alter the nature of guanine nucleotide regulation of adenylate cyclase. 相似文献
10.
A.A. Licata W.Y. Au J. Vera F.C. Bartter 《Biochimica et Biophysica Acta (BBA)/General Subjects》1979,582(1):59-66
We investigated some effects of prostaglandin E1 on the metabolism of rat parathyroid glands using a culture system containing basal Eagle's medium supplemented with 5–10% heat-inactivated rat serum. Rat parathyroid glands incorporate [3H]fucose and 14C-labeled amino acids into cellular glycoproteins and secrete some of these into the culture medium. Gel filtration chromatography separates these glycoproteins into three classes, the smallest of which (peak 3) is secreted with immunoreactive parathyroid hormone. In cultures of 48 h, prostaglandin E1 (1 μg/ml) specifically inhibits the secretion of peak 3 and of parathyroid hormone but has no effect on the incorporation of [3H]-fucose, 14C-labeled amino acids, or [3H]uridine into parathyroid glands. Cytochalasin B inhibits the secretion of parathyroid hormone and the incroporation of isotopic fucose and amino acids. Cortisol stimulates incorporation of [3H]fucose and the secretion of parathyroid hormone even in the presence of inhibitory doses of prostaglandin E1. It is concluded that, in organ culture, prostaglandin E1 inhibits the secretion of parathyroid hormone and of a specific glycoprotein the function of which may be related to the secretion of the hormone. 相似文献
11.
Laszlo G. Harsing Jr. Henry Sershen Sylvester E. Vizi Abel Lajtha 《Neurochemical research》1992,17(7):729-734
Mouse striatum was incubated with [3H]dopamine ([3H]DA) and superfused with and the tritium efflux induced by nicotine, electrical stimulation, or simultaneous nicotine and electrical stimulation was measured, to characterize the role of different Ca2+ channels in the transmitter release. Nicotine stimulation and electrical stimulation exerted additive effects on tritium efflux. Separation of the released radioactivity on alumina columns indicated that nicotine or electrical stimulation increases the release of [3H]DA and that the outflow of3H-labeled metabolites was similar with the two different stimulation procedures. Removal of Ca2+ from the superfusate resulted in a marked reduction in the tritium release evoked by nicotine, whereas the electrical stimulation-evoked tritium release was completely dependent on external Ca2+. The L-and N-type calcium channel blockers omega-conotoxin GVIA and Cd2+ inhibited the tritium release from the striatum evoked by either nicotine or electrical stimulation, whereas the L-type and T-type channel blockers diltiazem and Ni2+ did not alter release of [3H]DA. We conclude that N-type voltage-sensitive Ca2+ channels participate in striatal dopamine release, and we speculate that nicotinic receptor-operated ion channels permeable to cations such as Ca2+ and N-type voltage-sensitive calcium channels may simultaneously open up, and they additively increase free intracellular Ca2+ concentration. 相似文献
12.
Presynaptic modulation by eicosanoids in cortical synaptosomes 总被引:1,自引:0,他引:1
In continuing experiments to determine the ionic basis of inhibitory presynaptic modulation, rat cortical synaptosomes were employed and receptor-activated K+ efflux was determined with a K+ sensitive electrode. When synaptosomes were sub-optimally depolarized by veratridine, the addition of agents that activated purinergic, 2, muscarinic and opioid receptors all promoted K+ efflux. With 2-chloroadenosine as a model inhibitory presynaptic modulator, the increased K+ efflux evoked by this agent was blocked by the cyclooxygenase inhibitor indomethacin suggesting that arachidonic acid or its metabolites was an intermediary in opening the channel. When arachidonic acid and PGE2 were tested, both promoted K+ efflux that was inhibited by dendrotoxin and mast cell degranulating peptide, two agents that are known to inhibit a delayed rectifier K+ current. Our results suggest that via eicosanoid second messengers, inhibitory presynaptic modulators open a sub-class of K channels that hyperpolarize nerve terminals, therefore less Ca2+ would enter per nerve impulse and thus the evoked release of neurotransmitters would be decreased.Abbreviations DTX
dendrotoxin
- MCDP
mast cell degranulating peptide
- NHGA
norhydroguairetic acid
- PGE2
prostaglandin E2 相似文献
13.
J. MoskowitzJ.P. Harwood W.D. ReidG. Krishna 《Biochimica et Biophysica Acta (BBA)/General Subjects》1971
Prostaglandin E1 markedly increased the formation of cyclic [3H]AMP from labeled adenine in human and rabbit blood platelets. Norepinephrine alone had no stimulatory effect, but it reduced cyclic AMP levels elevated by prostaglandin E1. Phentolamine overcame the inhibitory effect of norepinephrine, whereas propranolol did not. Homogenization of platelets reduced, but did not abolish, the inhibitory effect of norepinephrine on adenyl cyclase activity induced by prostaglandin E1. 相似文献
14.
J. Van Sande P. Cochaux C. Decoster J.M. Boeynaems J.E. Dumont 《Biochimica et Biophysica Acta (BBA)/General Subjects》1982,716(1):53-60
Prostaglandins F1α and F2α, at high concentrations (≥28 μM) enhanced cyclic AMP accumulation in dog thyroid slices. At lower concentrations, they inhibited the cyclic AMP accumulation induced by thyrotropin (TSH), prostaglandin E1, and cholera toxin. This effect was rapid in onset and of short duration, calcium-dependent and suppressed by methylxanthines. Prostaglandin Fα also inhibited TSH-induced secretion and activated iodine binding to proteins. These characteristics are similar to those of carbamylcholine action, except that prostaglandins F did not enhance cyclic GMP accumulation. The effect of prostaglandin Fα was not inhibited by atropine, phentolamine and adenosine deaminase and can therefore not be ascribed to an induced secretion of acetylcholine, norepinephrine or adenosine. It is suggested that prostaglandins F act by increasing influx of extracellular Ca2+. Arachidonic acid also inhibited the TSH-induced cyclic AMP accumulation. However this effect was specific for TSH, it was enhanced in the absence of calcium and was not inhibited by methylxanthines or by indomethacin at concentrations which completely block its conversion to prostaglandin Fα. Arachidonic acid action is sustained. This suggests that arachidonic acid inhibits thyroid adenylate cyclase at the level of its TSH receptor and that this effect is not mediated by prostaglandin Fα or any other cyclooxygenase product. 相似文献
15.
16.
Lars Ove Farnebo 《Cell and tissue research》1971,122(4):503-519
Summary The effect of electrical field stimulation on noradrenaline (NA), dopamine (DA) and 5-hydroxytryptamine (5-HT) nerve terminals in rat brain slicesin vitro was investigated. Slices prepared from the cerebral cortex or the neostriatum were incubated in physiologic buffer for 30 min and then superfused by buffer and stimulated by an electrical field (biphasic pulses, 10 Hz, 12 mA, 2 ms) for various time periods. The effect of the stimulation was studied at the cellular level with the histochemical fluorescence technique of Falck and Hillarp. The transmitter overflow into the superfusing buffer caused by the stimulation was studied with isotope technique.
Cerebral Cortex NA Nerve Terminals. Stimulation caused release of NA from cortical NA nerve terminals. Already after 2 min stimulation a slight decrease of the fluorescence intensity of the nerve terminals could be found. Stimulation for 15 to 30 min greatly reduced the fluorescence intensity. In slices preincubated with3H-NA the stimulation-induced overflow of tritium during 2 min stimulation was about 15% (i.e. 15% of the tissue tritium content was overflowing into the superfusing buffer in response to stimulation for 2 min). During prolonged stimulation there was a considerable decline of the tritium efflux.
Cerebral Cortex 5-HT Nerve Terminals. The 5-HT-analogue 6-hydroxytryptamine (6-HT) which is readily taken up into 5-HT nerve terminals was used to permit good visualization of these nerve terminals. Uptake of 6-HT into cortical NA nerve terminals was prevented by preincubation with 6-hydroxydopamine (6-OH-DA) or protriptyline. Stimulation for 15 to 30 min reduced the fluorescence intensity of the 5-HT nerve terminals. In slices preincubated with3H-5-HT the stimulation-induced overflow of tritium during 2 min stimulation was about 5%. The tritium efflux slowly decreased during continuous stimulation.
Neostriatal DA Nerve Terminals. In slices frozen directly after preparation an intense diffuse fluorescence could be seen. After incubation in drug-free buffer at 37° C the fluorescence was localized in the varicosities of the DA nerve terminals. The central parts of the slices almost completely lacked specific fluorescence, while the outer zones were brightly fluorescent. No clear reduction of the fluorescence intensity of the DA nerve terminals in the outer zone could be observed after stimulation for 30 min. In slices preincubated with3H-DA the stimulation-induced overflow of tritium during 2 min stimulation was about 2%. The tritium efflux slowly decreased during continuous stimulation.It is suggested that the differences in release between the various nerve terminal systems foundin vitro reflect differences in transmitter release occurringin vivo. The comparably high release of NA per impulse from the cortical NA nerve terminals implicate that the discharge rate of these neuronsin vivo is very low.This investigation has been supported by grants from the Swedish Medical Research Council (B72-14X-2330-05A) and Magnus Bergwall's Foundation.The author is greatly indebted to Mrs. Annika Hamberger for her skillful technical assistance. For generous supplies of drugs thanks are due to Hässle, Göteborg, Sweden, through Dr. H. Corrodi (6-HT, 6-OH-DA and H44/68). 相似文献
17.
Prostaglandins E1 and E2 caused a 5–10 fold stimulation of ornithine decarboxylase activity in granulosa cells isolated from porcine ovarian follicles. The minimally effective concentration of prostaglandin E2 was 10 ng/ml and the plateau of activity was reached at 500 ng/ml. Prostaglandin F2α was ineffective. 1-Methyl,3-isobutyl-xanthine, a phosphodiesterase inhibitor, potentiated the effect of both submaximal and maximal effective doses of prostaglandin E2, suggesting that the effect of prostaglandin E2 is mediated by cAMP. The effect of prostaglandin E2 was similar to that of luteinizing hormone and a cAMP analogue, 8-Bromo-cAMP. 相似文献
18.
Edwin W. Salzman 《Biochimica et Biophysica Acta (BBA)/General Subjects》1977,499(1):48-60
The prostaglandin endoperoxide, prostaglandin G2, in platelet-rich plasma may produce reversible platelet aggregation without secretion, irreversible aggregation with secretion of platelet constituents inhibited by indomethacin, or the latter effects despite indomethacin, depending on the concentration of the endoperoxide. Irreversible aggregation and platelet secretion induced by prostaglandin G2 apparently result from the action of ADP, since these responses are inhibited by 2-n-amylthio-5′-AMP (an inhibitor of the actions of ADP on platelets) and they do not occur in heparinized platelet-rich plasma. Prostaglandin G2 lowers the platelet level of cyclic 3′,5′-AMP. Its actions are inhibited by elevation of cyclic AMP levels by prostaglandin E1 or dibutyryl cyclic AMP or adenosine. Like malondialdehyde production induced by thrombin, ADP, or arachidonic acid, prostaglandin G2-induced malondialdehyde production is reduced by dibutyryl cyclic AMP and prosraglandin E1. Platelet activation by prostaglandin G2 is enhanced by the adenylate cyclase inhibitor, 9-(tetrahydro-2-furyl)-adenine.The action of prostaglandin G2 on platelets is more complex then previously reported. 相似文献
19.
Srgio H. Ferreira Meire Nakamura Maria Salete de Abreu Castro 《Prostaglandins & other lipid mediators》1978,16(1):31-37
Hyperalgesia induced in rat paws or dog knee joints by prostacyclin (PGI2) and prostaglandin E2 was measured by a modification of the Randall-Selitto method (1) of by the degree of incapacitation (2). In both species PGI2 induced an immediate hyperalgesic effect but the effect of PGE2 had a longer latency. Low doses of PGI2 caused a short lasting effect but PGE2, large doses of PGI2 or successive administration of small doses of PGI2 caused a long lasting effect.It is suggested that prostacyclin mediates rat paw hyperalgesia induced by carrageenin. The long lasting hyperalgesic effect of PGE2 and high doses of PGI2 is possibly an indirect effect caused by stimulation of a sensory nerve sensitising mechanism. 相似文献
20.
Prostaglandins and cyclic AMP stimulate creatine kinase synthesis but not fusion in cultured embryonic chick muscle cells 总被引:1,自引:0,他引:1
Ulla B. Schützle Michael J.O. Wakelam Dirk Pette 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》1984,805(2):204-210
Cyclic AMP levels have been measured in cultures derived from 12-day-old chick embryonic muscle. A rise in concentration was found after the onset of myoblast fusion. Cells cultured at a medium Ca2+ concentration of 0.1 μM did not fuse and exhibited only a small rise in cyclic AMP concentration during culture. Addition of 1.4 mM Ca2+ to these cells after 50 h in culture caused rapid, synchronous fusion with a concomitant rise in cyclic AMP levels. Indomethacin, an inhibitor of prostaglandin synthesis, did not inhibit fusion, but inhibited the rise in cyclic AMP concentration. Indomethacin-treated cultures exhibited lower creatine kinase levels, though no change in the ratio of the three isoenzymes was observed. Addition of prostaglandins E1 and E2 to indomethacin-treated cultures overcame this inhibition. We propose that prostaglandin synthesis is a consequence of the stimulation of myoblast fusion and that via cyclic AMP it stimulates protein synthesis. 相似文献