Interleukin-12 is synthesized by mesangial cells and stimulates platelet-activating factor synthesis, cytoskeletal reorganization, and cell shape change. (1/947)
Preliminary studies indicate the involvement of interleukin (IL)-12 in experimental renal pathology. In the present study, we evaluated whether cultured glomerular mesangial cells are able to produce IL-12 and whether IL-12 may regulate some of their functions, including the cytoskeletal reorganization, the change in cell shape, and the production of platelet-activating factor (PAF). The results obtained indicate that pro-inflammatory stimuli, such as tumor necrosis factor-alpha and bacterial polysaccharides, induce the expression of IL-12 mRNA and the synthesis of the protein by cultured mesangial cells. Moreover, cultured mesangial cells were shown to bind IL-12 and to express the human low-affinity IL-12 beta1-chain receptor. When challenged with IL-12, mesangial cells produced PAF in a dose- and time-dependent manner and superoxide anions. No production of tumor necrosis factor-alpha and IL-8 was observed. Moreover, we demonstrate that IL-12 induced a delayed and sustained shape change of mesangial cells that reached its maximum between 90 and 120 minutes of incubation. The changes in cell shape occurred concomitantly with cytoskeletal rearrangements and may be consistent with cell contraction. As IL-12-dependent shape change of mesangial cells was concomitant with the synthesis of PAF, which is known to promote mesangial cell contraction, we investigated the role of PAF using two chemically different PAF receptor antagonists. Both antagonists inhibited almost completely the cell shape change induced by IL-12, whereas they were ineffective on angiotensin-II-induced cell shape change. In conclusion, our results suggest that mesangial cells can either produce IL-12 or be stimulated by this cytokine to synthesize PAF and to undergo shape changes compatible with cell contraction. (+info)Glutamate receptor signaling interplay modulates stress-sensitive mitogen-activated protein kinases and neuronal cell death. (2/947)
Glutamate receptors modulate multiple signaling pathways, several of which involve mitogen-activated protein (MAP) kinases, with subsequent physiological or pathological consequences. Here we report that stimulation of the N-methyl-D-aspartate (NMDA) receptor, using platelet-activating factor (PAF) as a messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal-regulated kinase, in primary cultures of hippocampal neurons. Activation of the metabotropic glutamate receptor (mGluR) blocks this NMDA-signaling through PAF and MAP kinases, and the resultant cell death. Recombinant PAF-acetylhydrolase degrades PAF generated by NMDA-receptor activation; the hetrazepine BN50730 (an intracellular PAF receptor antagonist) also inhibits both NMDA-stimulated MAP kinases and neuronal cell death. The finding that the NMDA receptor-PAF-MAP kinase signaling pathway is attenuated by mGluR activation highlights the exquisite interplay between glutamate receptors in the decision making process between neuronal survival and death. (+info)Differences in the actions of some blockers of the calcium-activated potassium permeability in mammalian red cells. (3/947)
1. The actions of some inhibitors of the Ca2+-activated K+ permeability in mammalian red cells have been compared. 2. Block of the permeability was assessed from the reduction in the net loss of K+ that followed the application of the Ca2+ ionophore A23187 (2 microM) to rabbit red cells suspended at a haematocrit of 1% in a low potassium solution ([K]0 0.12-0.17 mM) at 37 degrees C. Net movement of K+ was measured using a K+-sensitive electrode placed in the suspension. 3. The concentrations (microM +/- s.d.) of the compounds tested causing 50% inhibition of K+ loss were: quinine, 37 +/- 3; cetiedil, 26 +/- 1; the cetiedil congeners UCL 1269, UCL 1274 and UCL 1495, approximately 150, 8.2 +/- 0.1, 0.92 +/- 0.03 respectively; clotrimazole, 1.2 +/- 0.1; nitrendipine, 3.6 +/- 0.5 and charybdotoxin, 0.015 +/- 0.002. 4. The characteristics of the block suggested that compounds could be placed in two groups. For one set (quinine, cetiedil, and the UCL congeners), the concentration-inhibition curves were steeper (Hill coefficient, nH, > or = 2.7) than for the other (clotrimazole, nitrendipine, charybdotoxin) for which nH approximately 1. 5. Compounds in the first set alone became less active on raising the concentration of K+ in the external solution to 5.4 mM. 6. The rate of K+ loss induced by A23187 slowed in the presence of high concentrations of cetiedil and its analogues, suggesting a use-dependent component to the inhibitory action. This was not seen with clotrimazole. 7. The blocking action of the cetiedil analogue UCL 1274 could not be overcome by an increase in external Ca2+ and its potency was unaltered when K+ loss was induced by the application of Pb2+ (10 microM) rather than by A23187. 8. These results, taken with the findings of others, suggest that agents that block the red cell Ca2+-activated K+ permeability can be placed in two groups with different mechanisms of action. The differences can be explained by supposing that clotrimazole and charybdotoxin act at the outer face of the channel whereas cetiedil and its congeners may block within it, either at or near the K+ binding site that determines the flow of K+. (+info)Endothelin antagonists block alpha1-adrenergic constriction of coronary arterioles. (4/947)
We have previously observed that intracoronary administration of the alpha1-adrenergic agonist phenylephrine (PE) over a period of minutes induced both an immediate and long-lasting (2 h) vasoconstriction of epicardial coronary arterioles. Because it is unlikely that alpha1-adrenergic constriction would persist for hours after removal of the agonist, this observation supports the view that another constrictor(s) is released during alpha1-adrenergic activation and induces the prolonged vasoconstriction. Therefore, we hypothesized that the prolonged microvascular constriction after PE is due to the production of endothelin (ET). We focused on ET not only because this peptide produces potent vasoconstriction but also because its vasoconstrictor action is characterized by a long duration. To test this hypothesis, the diameters of coronary arterioles (<222 micrometers) in the beating heart of pentobarbital-anesthetized dogs with stroboscopic intravital microscopy were measured during a 15-min intracoronary infusion of PE (1 microgram. kg-1 . min-1) and at 15-min intervals for a total of 120 min. All experiments were performed in the presence of beta-adrenergic blockade with propranolol. At 120 min, arterioles in the PE group were constricted (-23 +/- 9% change in diameter vs. baseline). Pretreatment with the ET-converting enzyme inhibitor phosphoramidon or the ETA-receptor antagonist FR-139317 prevented the PE-induced constriction at 120 min (-1 +/- 3 and -6 +/- 3%, respectively, P < 0.01 vs. PE). Pretreatment with the selective alpha1-adrenergic antagonist prazosin (Prz) also prevented the sustained constriction (0 +/- 2%, P < 0.01 vs. PE) but Prz given 60 min after PE infusion did not (-13 +/- 3%). In the aggregate, these results show that vasoconstriction of epicardial coronary arterioles via alpha1-adrenergic activation is blocked by an ET antagonist and an inhibitor of its production. From these data, we conclude that alpha1-adrenergic activation promotes the production and/or release of ET, which produces or facilitates microvascular constriction of epicardial canine coronary arterioles. (+info)Mechanism of weight gain suppressing effect of ER-40133, an angiotensin I converting enzyme inhibitor, in growing rats. (5/947)
Effects of ER-40133, an inhibitor of angiotensin converting enzyme (ACE), on weight gain and sodium and potassium balance were studied in growing SD male rats. Thirty-two animals (seven weeks of age) were divided into two groups; one received a standard diet containing 0.227% sodium and the other a low (0.065%) sodium diet. They were divided into four subgroups; one control group and three treated groups receiving 3, 10 or 30 mg/kg of ER-40133, by gavage, once a day for five consecutive days. Body weight gain (average of the standard and low sodium diet groups) was -32% in the 3 mg/kg group,-74% in 10 mg/kg group and -99% in 30 mg/kg group, when compared with the control group. There was a highly linear correlation between suppression of body weight gain and reduction in sodium and potassium retention for both groups of animals given the standard and low sodium diet. The reduced sodium retention, the primary effect of ACE inhibitors, accounted for about 30% of suppressed weight gain, and the reduced potassium retention, the secondary effect of sodium deficiency, could account for the rest about 70% of weight suppression by ER-40133. (+info)Endothelin receptor expression and pharmacology in human saphenous vein graft. (6/947)
1. We have investigated the expression and pharmacology of endothelin (ET) receptors in human aortocoronary saphenous vein grafts. 2. Subtype-selective ligands were used to autoradiographically identify ET(A) ([125I]-PD151242) and ET(B)([125I]-BQ3020) receptors. In graft saphenous vein ETA receptors predominated in the media, with few ET(B) receptors identified. Neither subtype was detected in the thickened neointima. 3. The ratio of medial ET(A):ET(B) receptors was 75%: 25% in both graft and control saphenous vein. 4. ET-1 contracted control (EC50 2.9 nM) and graft (EC50 4.5 nM) saphenous vein more potently than diseased coronary artery (EC50 25.5 nM). 5. In all three blood vessels ET-1 was 100 times more potent than ET-3 and three times more potent than sarafotoxin 6b (S6b). Little or no response was obtained in any vessel with the ET(B) agonist sarafotoxin 6c (S6c). 6. The ET(A) antagonist PD156707 (100 nM) blocked ET-1 responses in all three vessels with pKb values of approximately 8.0. 7. For individual graft veins the EC50 value for ET-1 and 'age' of graft in years showed a significant negative correlation. 8. In conclusion there is no alteration in ET receptor expression in the media of saphenous veins grafted into the coronary circulation compared to control veins. ETA receptors predominantly mediate the vasoconstrictor response to ET-1 in graft vein, with no apparent up-regulation of ET(B) receptors. The sensitivity of the graft vein to ET-1 increased with graft 'age', suggesting that these vessels may be particularly vulnerable to the increased plasma ET levels that are detected in patients with cardiovascular disease. (+info)Pharmacological and molecular biological evidence for ETA endothelin receptor subtype mediating mechanical responses in the detrusor smooth muscle of the human urinary bladder. (7/947)
The aim of this study was to characterize endothelin receptor subtypes of the detrusor muscle of the human urinary bladder. The receptor subtypes mediating endothelin (ET)-1-induced activity in the human detrusor smooth muscles have been characterized using isometric contraction and reverse transcription-polymerase chain reaction (RT-PCR). ET-1 (a non-selective ET receptor agonist; 10(-10) M to 10(-6) M) exhibited concentration-dependent contractions in human urinary bladder with a plateau at concentrations above 3x10(-7) M. Neither IRL1620 nor sarafotoxin S6c (both ETB-selective agonists; 10(-10) M to 10(-6) M) elicited contractile activity in the human urinary bladder detrusor smooth muscle. FR139317 (an ETA-selective antagonist; 10(-7) M to 10(-5) M) produced a marked shift to the right of the ET-1 concentration-response curve in human urinary bladder detrusor smooth muscle (from the Schild plot TpA2=7.96; slope=0.95). In contrast, RES701-1 (an ETB-selective antagonist; 10(-7) M to 10(-5) M) had no effect on the ET-1 concentration-response curve. RT-PCR revealed positive amplification of ETA receptor mRNA fragment, but not ETB. These results indicate that the ET-1-induced contractile effects of urinary bladder detrusor smooth muscle seem to be mediated mainly by the ETA receptor, not by the ETB receptor. (+info)Influence of platelet-activating factor on cerebral microcirculation in rats: part 1. Systemic application. (8/947)
BACKGROUND AND PURPOSE: Platelet-activating factor (PAF) has been demonstrated to have a mediator function in shock, with some of its deleterious effects being attributed to its influence on microcirculation. Systemic PAF concentrations as found in shock could also compromise the cerebral microcirculation. Our purpose in the present study was to examine the influence of systemically applied PAF on microvascular perfusion and leukocyte-endothelium interactions in cerebral microvessels. METHODS: A closed cranial window technique was used for intravital fluorescence microscopy of the brain surface. PAF was infused in concentrations of 10(-12), 10(-9), and 10(-6) mol/L into the carotid artery (5 mL/h for 20 min) of Sprague-Dawley rats (n=30). The selective PAF receptor antagonist WEB 2170BS (2 mg/kg body weight) was used to inhibit specific PAF effects. RESULTS: The number of leukocytes (cells/100 microm. min) rolling along or adhering at the venular endothelium increased following infusion of PAF 10(-6) mol/L from 7.7+/-2.5 to 24.4+/-8.9 (P<0.05) and from 1.9+/-0.5 to 6.9+/-2.2 (P<0.05), respectively, within 2 hours. Mean arterial pressure decreased from 92+/-22 mm Hg to 49+/-17 mm Hg (P<0.05). The lower concentrations of PAF were less effective to decrease mean arterial pressure but also induced leukocyte-endothelium interactions. The intravenous administration of WEB 2170BS 15 min before the infusion of PAF 10(-6) mol/L prevented both systemic hypotension and activation of leukocyte-endothelium interactions. CONCLUSIONS: Increased systemic blood levels of PAF as found during shock can not only cause systemic arterial hypotension but also induce leukocyte-endothelium interactions in cerebral venules. The activation of leukocytes was found to be independent of PAF-induced arterial hypotension. The specificity of these results is confirmed by the findings that WEB 2170BS could inhibit the PAF-induced systemic hypotension as well as the activation of leukocytes. (+info)
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Azepine
Azepines are unsaturated heterocycles of seven atoms, with a nitrogen replacing a carbon at one position. Azepane Benzazepines ... Azepines, All stub articles, Heterocyclic compound stubs). ...
Azepane
Azepine "Hexamethyleneimine". Karsten Eller, Erhard Henkes, Roland Rossbacher, Hartmut Höke (2005). "Amines, Aliphatic". ...
Heterocyclic compound
For azepine, benzazepine is the preferred name. Likewise, the compounds with two benzene rings fused to the central heterocycle ...
Imipramine
... azepine (dibenzazepine), was first synthesized in 1899, but no pharmacological assessment of this compound or any substituted ... azepines; key synthons in syntheses of pharmaceutically active compounds". Journal of Heterocyclic Chemistry. 36 (1): 57-64. ...
Solenopsin
O'Hagan, David (1997). "Pyrrole, pyrrolidine pyridine, piperidine, azepine and tropane alkaloids". Natural Product Reports ( ...
Pinnatoxin
Ion channel toxins, Neurotoxins, Invertebrate toxins, Cyclohexenes, Azepines, Spiro compounds, Tetrahydropyrans, ...
Osanetant
January 2013). "Azepines and piperidines with dual norepinephrine dopamine uptake inhibition and antidepressant activity". ACS ...
Azomethine ylide
Nedolya, N. A.; Trofimov, B. A. (2013). "[1,7]-Electrocyclization reactions in the synthesis of azepine derivatives". Chemistry ...
5-HT6 receptor
"Tricyclic azepine derivatives as selective brain penetrant 5-HT6 receptor antagonists". Bioorganic & Medicinal Chemistry ...
Azonine
Azepine Pyrrole Cyclononatetraene (2Z,4Z,6Z,8Z)-Thionine Oxonine Somers, K. R. F.; Kryachko, E. S.; Ceulemans, A. (2004). " ...
Flupyradifurone
... azepine alkaloids and related derivatives from Stemona species". Phytochemistry. 63 (7): 803-816. doi:10.1016/s0031-9422(03) ... azepine Stemona Alkaloid". Journal of Natural Products. 67 (4): 675-677. doi:10.1021/np034066u. ISSN 0163-3864. PMID 15104502 ...
José Barluenga
Synthesis of Azepines and Mechanistic NMR Studies". Chemistry: A European Journal. 2: 88-97. doi:10.1002/chem.19960020116. ...
Benzazepine
... s are heterocyclic chemical compounds consisting of a benzene ring fused to an azepine ring. Examples include: ...
Dibenzazepine
... (iminostilbene) is a chemical compound with two benzene rings fused to an azepine group. Benzazepine ...
Solar chemical
Various ketones, azepines and norbornadienes among other compounds, such as azobenzene and its derivatives, have been ...
5-HT2A receptor
LY-367,265 - dual 5-HT2A antagonist / SSRI with antidepressant effects 2-alkyl-4-aryl-tetrahydro-pyrimido-azepines are subtype ...
Divinylcyclopropane-cycloheptadiene rearrangement
Divinyl aziridines undergo a similar suite of reactions providing azepines or vinyl pyrrolines depending on the relative ...
Alfred Hassner
... as well as of larger ring heterocycles including azepines. Recently they studied TiCl 4 {\displaystyle _{4}} catalyzed ...
5-HT2C receptor agonist
... azepines as potent and selective 5-HT2C receptor agonists: Design, synthesis, and evaluation of PF-3246799 as a treatment for ...
Fluperlapine
... (NB 106-689), also known as fluoroperlapine, is a morphanthridine (11H-dibenzo[b,e]azepine) atypical antipsychotic ...
CR gas
Molecular modeling studies on 11H-dibenz[b,e]azepine and dibenz[b,f][1,4]oxazepine derivatives as potent agonists of the human ...
Dianicline
Azepines, Bridged heterocyclic compounds, Pyridines). ...
Stevensine
Azepines, Bromoarenes, Imidazoles, Pyrroles). ...
PF-04479745
June 2014). "Multiparameter optimization in CNS drug discovery: design of pyrimido[4,5-d]azepines as potent 5-hydroxytryptamine ...
5-HT2C receptor
June 2014). "Multiparameter optimization in CNS drug discovery: design of pyrimido[4,5-d]azepines as potent 5-hydroxytryptamine ...
Tabernanthine
Azepines, Quinuclidine alkaloids, Tryptamine alkaloids, All stub articles, Nervous system drug stubs). ...
PNU-22394
Azepines, Tryptamines, All stub articles, Nervous system drug stubs). ...
Controlled Drugs and Substances Act
... ethyl hexahydro-1-methyl-4-phenyl-azepine-4-carboxylate) and its salts Metethoheptazine (ethyl hexahydro-1,3-dimethyl-4- ...
Galantamine total synthesis
... galanthamine 9 the hydroxyl group is activated as the triflate and the amine group as the mesylate for intramolecular azepine ...
Ketipramine
It differs from imipramine in terms of chemical structure only by the addition of a ketone group, to the azepine ring, and is ...
1H-AZEPINE, HEXAHYDRO-1-((2-FURYLDIMETHYLSILYL)METHYL)-, HYDROCHLORIDE
1-Methyl-7-(methylsulfanyl)-2,3,4,5-tetrahydro-1H-azepine | C8H15NS | ChemSpider
Ring-Expansion Reactions of Binaphthyl Azepines and Ferrocenophanes through Metal-Catalyzed [1,2]-Stevens... | Archive ouverte...
HARTHONG, Steven et al. Ring-Expansion Reactions of Binaphthyl Azepines and Ferrocenophanes through Metal-Catalyzed [1,2]- ... Ring-Expansion Reactions of Binaphthyl Azepines and Ferrocenophanes through Metal-Catalyzed [1,2]-Stevens Rearrangements. ... Ring-Expansion Reactions of Binaphthyl Azepines and Ferrocenophanes through Metal-Catalyzed [1,2]-Stevens... ... binaphthyl azocines can be prepared in a single step via the direct copper-catalyzed reaction of binaphthyl azepines and α- ...
methyl 1,2,4,5-tetrahydro-3H-naphtho[2,3-d]azepine-3-carboxylate - C16H17NO2, density, melting point, boiling point, structural...
... azepine-3-carboxylate - C16H17NO2, synthesis, structure, density, melting point, boiling point ... azepine-3-carboxylate , density of methyl 1,2,4,5-tetrahydro-3H-naphtho[2,3-d]azepine-3-carboxylate , refractive index of ... Tags: melting point of methyl 1,2,4,5-tetrahydro-3H-naphtho[2,3-d]azepine-3-carboxylate , boiling point of methyl 1,2,4,5- ... methyl 1,2,4,5-tetrahydro-3H-naphtho[2,3-d]azepine-3-carboxylate. ...
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Nucleophilic Substitution Reaction of 5-tert-Butyl-2-methoxy-3H-azepine by an Alkoxide Ion and Alkyllithium Reagent: Unexpected...
Satake K. Nucleophilic Substitution Reaction of 5-tert-Butyl-2-methoxy-3H-azepine by an Alkoxide Ion and Alkyllithium Reagent: ... Satake, K. (2002). Nucleophilic Substitution Reaction of 5-tert-Butyl-2-methoxy-3H-azepine by an Alkoxide Ion and Alkyllithium ... Satake, K 2002, Nucleophilic Substitution Reaction of 5-tert-Butyl-2-methoxy-3H-azepine by an Alkoxide Ion and Alkyllithium ... title = "Nucleophilic Substitution Reaction of 5-tert-Butyl-2-methoxy-3H-azepine by an Alkoxide Ion and Alkyllithium Reagent: ...
Acid exposure stimulates the adherence of Streptococcus pneumoniae to cultured human airway epithelial cells: effects on...
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Registration Dossier - ECHA
N,N-hexane-1,6-diylbis(hexahydro-2-oxo-1H-azepine-1-carboxamide) EC Number:. 227-563-7. EC Name:. N,N-hexane-1,6-diylbis( ... N,N-hexane-1,6-diylbis(hexahydro-2-oxo-1H-azepine-1-carboxamide)azepine-1-carboxamide)azepine-1-carboxamide)
Hexamethylenimine
Remeron (Mirtazapine): Uses, Dosage, Side Effects, Interactions, Warning
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Chapter 893 Section 03 - 2019 Florida Statutes - The Florida Senate
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BJOC - Synthesis of 2,1-benzisoxazole-3(1H)-ones by base-mediated photochemical N-O bond-forming cyclization of 2-azidobenzoic...
Interestingly, under these conditions (Table 3), the yields for 3H-azepine 3a and 3c were determined as 20 and 18%, ... Meanwhile a molecular form of 1 produced azepine 3 (path II) by irradiation. The detailed mechanism of the formation of 3 is ... In the past, research has been focused on the formation of 2-substituted 3H-azepines 3 as products of the photolysis or ... After this, the conversion of 1c (according to HPLC monitoring) was found to be 100% and azepine 3c was isolated after ...
Carbamazepine: Uses, Interactions, Mechanism of Action | DrugBank Online
These are compounds with two benzene rings connected by an azepine ring. Azepine is an unsaturated seven-member heterocycle ... Azepines / Benzenoids / Ureas / Azacyclic compounds / Organopnictogen compounds / Organonitrogen compounds / Organic oxides / ... Aromatic heteropolycyclic compound / Azacycle / Azepine / Benzenoid / Carbonic acid derivative / Carbonyl group / Dibenzazepine ...
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Azepines Preferred Term Term UI T004046. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1966). ... Azepines Preferred Concept UI. M0002069. Registry Number. 0. Scope Note. Seven membered heterocyclic rings containing a ... Azepines. Tree Number(s). D03.383.066. Unique ID. D001381. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/D001381 Scope Note ...