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[PMID]: 26461804
[Au] Autor:Saxena M; Bhunia SS; Saxena AK
[Ad] Address:a Department of Chemistry , Amity University , Lucknow , India.
[Ti] Title:Molecular modelling studies on 2-substituted octahydropyrazinopyridoindoles for histamine H2 receptor antagonism.
[So] Source:SAR QSAR Environ Res;26(7-9):739-55, 2015.
[Is] ISSN:1029-046X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The human histamine H2 receptor (hH2HR) is a G-protein coupled receptor protein with seven transmembrane (TM)-spanning helices primarily involved in regulation of gastric acid secretion. Antagonists targeting hH2HR are useful in the treatment of hyperacidic conditions such as peptic ulcers, gastresophageal reflux disease and gastrointestinal bleeding. We have previously reported the antagonism of 2-substituted pyrazinopyridoindoles at the human histamine H1 receptor and mode of binding of these compounds at the hH1HR using in silico methods. Interestingly, some of the compounds in the series also showed promising activity towards hH2HR that prompted us to investigate the mode of binding of these compounds at hH2HR. In the absence of the crystal structure of hH2HR a homology model has been constructed using multiple sequence alignment, using the X-ray crystal structures of Turkey ß1-adrenergic receptor (tß1AR), Human histamine H1 receptor (hH1HR), Human ß2-adrenergic receptor (hß2AR) and Human D3 dopamine receptor (hD3R). The important residues for binding were depicted in TMIII, TMV, TMVI and TMVII by the homology modelled hH2HR for 2-substituted pyrazinopyridoindoles. A comparative study for deducing the selectivity regarding the binding towards hH1HR and hH2HR has been carried out, which may be useful in designing of selective hH1HR/hH2HR antagonists in these classes of compounds.
[Mh] MeSH terms primary: Histamine H2 Antagonists/chemistry
Receptors, Histamine H2/chemistry
[Mh] MeSH terms secundary: Cimetidine/chemistry
Computer Simulation
Famotidine/chemistry
Humans
Indoles/chemistry
Metiamide/chemistry
Molecular Docking Simulation
Pyrazines/chemistry
Pyridines/chemistry
Ranitidine/chemistry
Sequence Homology, Amino Acid
Structure-Activity Relationship
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Histamine H2 Antagonists); 0 (Indoles); 0 (Pyrazines); 0 (Pyridines); 0 (Receptors, Histamine H2); 3K7670861M (Metiamide); 5QZO15J2Z8 (Famotidine); 80061L1WGD (Cimetidine); 884KT10YB7 (Ranitidine)
[Em] Entry month:1612
[Cu] Class update date: 161230
[Lr] Last revision date:161230
[Js] Journal subset:IM
[Da] Date of entry for processing:151014
[St] Status:MEDLINE
[do] DOI:10.1080/1062936X.2015.1088572

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[PMID]: 20978923
[Au] Autor:Ganellin CR
[Ad] Address:Department of Chemistry, University College London, Christopher Ingold Laboratories, 20 Gordon Street, London WC1H 0AJ, UK. c.r.ganellin@ucl.ac.uk
[Ti] Title:Personal reflections on Sir James Black (1924-2010) and histamine.
[So] Source:Inflamm Res;60(1):103-10, 2011 Jan.
[Is] ISSN:1420-908X
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Sir James Black, Nobel laureate (1988), became interested in the role of histamine in gastric acid secretion in the early 1950s. In 1964, he joined the pharmaceutical company Smith Kline and French Laboratories at their English subsidiary to seek a new type of antagonist that would block those actions of histamine that were not blocked by mepyramine. No such compound was known and working with medicinal chemists it took four years to discover a lead compound. Further work provided the compound burimamide, which was used to define histamine H(2) receptors in 1972 for the first time, and to verify the action in human volunteers. Subsequent work led to the drug metiamide, which was withdrawn during early clinical trials. This was replaced by cimetidine, which was launched in 1977, as the first histamine H(2)-receptor antagonist and which revolutionized the treatment of peptic ulcer disease. The characterisation of a second type of histamine receptor revitalised interest in histamine and led to many later studies on the role of histamine in inflammation.
[Mh] MeSH terms primary: Histamine
Research Personnel
[Mh] MeSH terms secundary: Animals
Drug Discovery
Gastric Juice/secretion
Histamine Antagonists/chemistry
Histamine Antagonists/history
History, 20th Century
Humans
Molecular Structure
Nobel Prize
Receptors, Histamine/metabolism
[Pt] Publication type:HISTORICAL ARTICLE; JOURNAL ARTICLE
[Nm] Name of substance:0 (Histamine Antagonists); 0 (Receptors, Histamine); 820484N8I3 (Histamine)
[Em] Entry month:1104
[Cu] Class update date: 170718
[Lr] Last revision date:170718
[Js] Journal subset:IM
[Da] Date of entry for processing:101028
[St] Status:MEDLINE
[do] DOI:10.1007/s00011-010-0269-2

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[PMID]: 18184767
[Au] Autor:Matsumoto I; Inoue Y; Shimada T; Matsunaga T; Aikawa T
[Ad] Address:Department of Physiology, Nagasaki University School of Medicine, Nagasaki 852-8523, Japan. matu-itu@net.nagasaki-u.ac.jp
[Ti] Title:Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs.
[So] Source:Am J Physiol Regul Integr Comp Physiol;294(3):R689-98, 2008 Mar.
[Is] ISSN:0363-6119
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Because degranulation of brain mast cells activates adrenocortical secretion (41, 42), we examined whether activation of such cells increases renin and vasopressin (antidiuretic hormone: ADH) secretion. For this, we administered compound 48/80 (C48/80), which liberates histamine from mast cells, to pentobarbital-anesthetized dogs. An infusion of 37.5 microg/kg C48/80 into the cerebral third ventricle evoked increases in plasma renin activity (PRA), and in plasma epinephrine (Epi) and ADH concentrations. Ketotifen (mast cell-stabilizing drug; given orally for 1 wk before the experiment) significantly reduced the C48/80-induced increases in PRA, Epi, and ADH. Resection of the bilateral splanchnic nerves (SPX) below the diaphragm completely prevented the C48/80-induced increases in PRA and Epi, but potentiated the C48/80-induced increase in ADH and elevated the plasma Epi level before and after C48/80 challenge. No significant changes in mean arterial blood pressure, heart rate, concentrations of plasma electrolytes (Na+, K+, and Cl-), or plasma osmolality were observed after C48/80 challenge in dogs with or without SPX. Pyrilamine maleate (H1 histaminergic-receptor antagonist) significantly reduced the C48/80-induced increase in PRA when given intracerebroventricularly, but not when given intravenously. In contrast, metiamide (H2 histaminergic-receptor antagonist) given intracerebroventricularly significantly potentiated the C48/80-induced PRA increase. A small dose of histamine (5 microg/kg) administered intracerebroventricularly increased PRA twofold and ADH fourfold (vs. their basal level). These results suggest that in dogs, endogenous histamine liberated from brain mast cells may increase renin and Epi secretion (via the sympathetic outflow) and ADH secretion (via the central nervous system).
[Mh] MeSH terms primary: Brain Chemistry/drug effects
Brain/cytology
Histamine Release/drug effects
Mast Cells/drug effects
Mast Cells/metabolism
Renin/metabolism
Vasopressins/metabolism
p-Methoxy-N-methylphenethylamine/pharmacology
[Mh] MeSH terms secundary: Animals
Catecholamines/blood
Cell Degranulation/drug effects
Dogs
Drug Synergism
Histamine H1 Antagonists/pharmacology
Histamine H2 Antagonists/pharmacology
Injections, Intraventricular
Ketotifen/pharmacology
Kidney/drug effects
Kidney/physiology
Male
Splanchnic Nerves/physiology
Stimulation, Chemical
p-Methoxy-N-methylphenethylamine/administration & dosage
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Catecholamines); 0 (Histamine H1 Antagonists); 0 (Histamine H2 Antagonists); 11000-17-2 (Vasopressins); 4091-50-3 (p-Methoxy-N-methylphenethylamine); EC 3.4.23.15 (Renin); X49220T18G (Ketotifen)
[Em] Entry month:0810
[Cu] Class update date: 131121
[Lr] Last revision date:131121
[Js] Journal subset:IM
[Da] Date of entry for processing:080111
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00453.2007

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[PMID]: 17332265
[Au] Autor:Preuss H; Ghorai P; Kraus A; Dove S; Buschauer A; Seifert R
[Ad] Address:Department of Pharmaceutical/Medicinal Chemistry II, Institute of Pharmacy, University of Regensburg, Regensburg, Germany.
[Ti] Title:Constitutive activity and ligand selectivity of human, guinea pig, rat, and canine histamine H2 receptors.
[So] Source:J Pharmacol Exp Ther;321(3):983-95, 2007 Jun.
[Is] ISSN:0022-3565
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Previous studies revealed pharmacological differences between human and guinea pig histamine H(2) receptors (H(2)Rs) with respect to the interaction with guanidine-type agonists. Because H(2)R species variants are structurally very similar, comparative studies are suited to relate different properties of H(2)R species isoforms to few molecular determinants. Therefore, we systematically compared H(2)Rs of human (h), guinea pig (gp), rat (r), and canine (c). Fusion proteins of hH(2)R, gpH(2)R, rH(2)R, and cH(2)R, respectively, and the short splice variant of G(salpha), G(salphaS), were expressed in Sf9 insect cells. In the membrane steady-state GTPase activity assay, cH(2)R-G(salphaS) but neither gpH(2)R-G(salphaS) nor rH(2)R-G(salphaS) showed the hallmarks of increased constitutive activity compared with hH(2)R-G(salphaS), i.e., increased efficacies of partial agonists, increased potencies of agonists with the extent of potency increase being correlated with the corresponding efficacies at hH(2)R-G(salphaS), increased inverse agonist efficacies, and decreased potencies of antagonists. Furthermore, in membranes expressing nonfused H(2)Rs without or together with mammalian G(salphaS) or H(2)R-G(salpha) fusion proteins, the highest basal and GTP-dependent increases in adenylyl cyclase activity were observed for cH(2)R. An example of ligand selectivity is given by metiamide, acting as an inverse agonist at hH(2)R-G(salphaS), gpH(2)R-G(salphaS), and rH(2)R-G(salphaS) in the GTPase assay in contrast to being a weak partial agonist with decreased potency at cH(2)R-G(salphaS). In conclusion, the cH(2)R exhibits increased constitutive activity compared with hH(2)R, gpH(2)R, and rH(2)R, and there is evidence for ligand-specific conformations in H(2)R species isoforms.
[Mh] MeSH terms primary: Histamine Agonists/pharmacology
Histamine H2 Antagonists/pharmacology
Receptors, Histamine H2/metabolism
[Mh] MeSH terms secundary: Adenylyl Cyclases/metabolism
Animals
Baculoviridae/genetics
Cell Line
Cell Membrane/drug effects
Cell Membrane/metabolism
Dogs
GTP Phosphohydrolases/metabolism
GTP-Binding Protein alpha Subunits, Gs/genetics
GTP-Binding Protein alpha Subunits, Gs/metabolism
Guinea Pigs
Histamine/pharmacology
Humans
Ligands
Metiamide/pharmacology
Rats
Receptors, Histamine H2/genetics
Recombinant Fusion Proteins/metabolism
Recombinant Proteins/metabolism
Species Specificity
Spodoptera
Transfection
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Histamine Agonists); 0 (Histamine H2 Antagonists); 0 (Ligands); 0 (Receptors, Histamine H2); 0 (Recombinant Fusion Proteins); 0 (Recombinant Proteins); 3K7670861M (Metiamide); 820484N8I3 (Histamine); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gs); EC 4.6.1.1 (Adenylyl Cyclases)
[Em] Entry month:0707
[Cu] Class update date: 151119
[Lr] Last revision date:151119
[Js] Journal subset:IM
[Da] Date of entry for processing:070303
[St] Status:MEDLINE

  5 / 930 MEDLINE  
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[PMID]: 15231494
[Au] Autor:Matsumoto I; Inoue Y; Tsuchiya K; Shimada T; Aikawa T
[Ad] Address:Dept. of Physiology, Nagasaki Univ. School of Medicine, Nagasaki 852-8523, Japan. matu-itu@net.nagasaki-u.ac.jp
[Ti] Title:Degranulation of mast cells located in median eminence in response to compound 48/80 evokes adrenocortical secretion via histamine and CRF in dogs.
[So] Source:Am J Physiol Regul Integr Comp Physiol;287(4):R969-80, 2004 Oct.
[Is] ISSN:0363-6119
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The effect of intracerebroventricular infusion of compound 48/80 (C48/80), a mast cell secretagogue, on adrenal cortisol secretion was investigated in dogs under pentobarbital sodium anesthesia. A marked increase in adrenal cortisol secretion was elicited by C48/80 along with a concomitant increase in the plasma levels of cortisol and immunoreactive ACTH, but neither arterial blood pressure and heart rate nor the plasma histamine level altered significantly. Pretreatment with either anti-CRF antiserum or pyrilamine maleate (H(1) histamine-receptor antagonist) significantly attenuated the C48/80-evoked increase in cortisol secretion, but pretreatment with metiamide (H(2)-receptor antagonist) significantly potentiated it. Significant attenuation of the C48/80-evoked increase in cortisol also occurred in dogs given ketotifen, a mast cell stabilizing drug, before pharmacologic challenge. In the pars tuberalis and median eminence (ME), mast cells were highly concentrated in close association with the primary plexus of the hypophysial portal system. Degranulated mast cells were extensively found in the ME of C48/80-treated animals. These results suggest that mast cells located in these regions liberated histamine within the brain as a result of degranulation induced by C48/80 and that this led to activation of the hypothalamic-pituitary-adrenocortical axis.
[Mh] MeSH terms primary: Adrenal Cortex/secretion
Cell Degranulation/drug effects
Corticotropin-Releasing Hormone/physiology
Histamine/physiology
Median Eminence/cytology
Median Eminence/drug effects
p-Methoxy-N-methylphenethylamine/pharmacology
[Mh] MeSH terms secundary: Adrenal Cortex/drug effects
Adrenocorticotropic Hormone/pharmacology
Animals
Chromatography, Thin Layer
Dogs
Dose-Response Relationship, Drug
Epinephrine/pharmacology
Female
Hemodynamics/drug effects
Histamine/blood
Histamine H1 Antagonists/pharmacology
Histamine H2 Antagonists/pharmacology
Hydrocortisone/blood
Hydrocortisone/secretion
Injections, Intraventricular
Ketotifen/pharmacology
Male
Metiamide/pharmacology
Pyrilamine/pharmacology
Splanchnic Circulation/physiology
p-Methoxy-N-methylphenethylamine/administration & dosage
p-Methoxy-N-methylphenethylamine/antagonists & inhibitors
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Histamine H1 Antagonists); 0 (Histamine H2 Antagonists); 3K7670861M (Metiamide); 4091-50-3 (p-Methoxy-N-methylphenethylamine); 820484N8I3 (Histamine); 9002-60-2 (Adrenocorticotropic Hormone); 9015-71-8 (Corticotropin-Releasing Hormone); HPE317O9TL (Pyrilamine); WI4X0X7BPJ (Hydrocortisone); X49220T18G (Ketotifen); YKH834O4BH (Epinephrine)
[Em] Entry month:0410
[Cu] Class update date: 131121
[Lr] Last revision date:131121
[Js] Journal subset:IM
[Da] Date of entry for processing:040703
[St] Status:MEDLINE

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[PMID]: 12954791
[Au] Autor:Sundström E; Låstbom L; Ryrfeldt A; Dahlén SE
[Ad] Address:Division of Physiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
[Ti] Title:Interactions among three classes of mediators explain antigen-induced bronchoconstriction in the isolated perfused and ventilated guinea pig lung.
[So] Source:J Pharmacol Exp Ther;307(1):408-18, 2003 Oct.
[Is] ISSN:0022-3565
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Intravascular challenge of isolated perfused and ventilated guinea pig lung (IPL) from actively sensitized guinea pigs, with cumulatively increasing (10-10,000 microg) doses of ovalbumin (OVA), resulted in dose-dependent and reproducible reductions in lung conductance. The antihistamines mepyramine (1 microM) and metiamide (1 microM), the leukotriene antagonist zafirlukast (0.1 microM), or the cyclooxygenase enzyme (COX) inhibitor diclofenac (10 microM) each caused a parallel and rightward shift in the dose-response relation for OVA, providing evidence for contributions of histamine, cysteinyl-leukotrienes, and COX products to the OVA-induced bronchoconstriction in the IPL. Moreover, when all three drugs were combined there was a complete abolishment of the response to OVA. When two antagonists or inhibitors were combined, the results, however, were more complex. The 5-lipoxygenase inhibitor BAY x1005 (30 microM) and the thromboxane (TP) receptor antagonist BAY u3405 (1 microM) given as single treatment did not inhibit the response to OVA. However, combinations of different antagonists/inhibitors, including BAY x1005 and BAY u3405, caused pronounced inhibitions of the antigen responses, suggesting synergism in action. On the basis of these data it was concluded that although histamine and cysteinyl-leukotrienes mediate the major part of the bronchoconstriction, one or several prostanoids other than thromboxane contribute to the bronchoconstriction evoked by OVA. Moreover, the effect of diclofenac involved a dual action because it also made the IPL less sensitive to histamine and LTD4. The findings resemble and extend recent observations in clinical studies of patients with asthma and support the usefulness of this particular model in airway pharmacology.
[Mh] MeSH terms primary: Bronchoconstriction/drug effects
Cysteine/pharmacology
Histamine/pharmacology
Leukotrienes/pharmacology
Lung/drug effects
Ovalbumin
[Mh] MeSH terms secundary: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid/pharmacology
Animals
Bronchoconstriction/physiology
Drug Interactions
Guinea Pigs
Histamine Antagonists/pharmacology
Leukotriene D4/pharmacology
Lung/physiology
Male
Perfusion
Pyrilamine/pharmacology
Thromboxanes/chemistry
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Histamine Antagonists); 0 (Leukotrienes); 0 (Thromboxanes); 0 (cysteinyl-leukotriene); 73836-78-9 (Leukotriene D4); 76898-47-0 (15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid); 820484N8I3 (Histamine); 9006-59-1 (Ovalbumin); HPE317O9TL (Pyrilamine); K848JZ4886 (Cysteine)
[Em] Entry month:0310
[Cu] Class update date: 131121
[Lr] Last revision date:131121
[Js] Journal subset:IM
[Da] Date of entry for processing:030905
[St] Status:MEDLINE

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[PMID]: 11191621
[Au] Autor:Scaccianoce S; Lombardo K; Nicolai R; Affricano D; Angelucci L
[Ad] Address:Department of Human Physiology and Pharmacology, University La Sapienza, Rome, Italy. scaccianoce@uniroma1.it
[Ti] Title:Studies on the involvement of histamine in the hypothalamic-pituitary-adrenal axis activation induced by nerve growth factor.
[So] Source:Life Sci;67(26):3143-52, 2000 Nov 17.
[Is] ISSN:0024-3205
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Nerve growth factor (NGF) has been shown to stimulate the hypothalamic-pituitary-adrenocortical (HPA) axis. Since NGF induces the release of histamine from mast cells and in consideration of the fact that histamine is an HPA axis activator, we investigated whether NGF adrenocortical stimulation is mediated by histamine. To accomplish with it, the H1 histamine antagonist promethazine and the H2 antagonists metiamide and zolantidine were used in freely-moving cannulated rats. The increase in plasma corticosterone concentration induced by histamine administration was prevented completely by promethazine pretreatment but was unaffected by the H2 antagonists. Neither H1 nor H2 antagonists affected the adrenocortical stimulation induced by NGF administration. Moreover, since mast cells are reportedly present in the rat adrenal gland and the locally released histamine mediates the release of adrenaline which, in turn, stimulates glucocorticoid synthesis and secretion, we studied the effect of NGF on basal and ACTH-stimulated corticosterone release from in vitro isolated quartered adrenal glands and collagenase-dispersed adrenal cells. The results from these in vitro experiments have indicated that NGF modified neither spontaneous nor stimulated corticosterone release. Altogether these observations suggest that endogenous histamine is unlikely to be involved in HPA axis stimulation by NGF and reinforce the previously proposed concept of an active participation of NGF in the control of adrenocortical activity.
[Mh] MeSH terms primary: Histamine/physiology
Hypothalamo-Hypophyseal System/physiology
Nerve Growth Factor/physiology
Pituitary-Adrenal System/physiology
[Mh] MeSH terms secundary: Adrenal Glands/metabolism
Animals
Benzothiazoles
Catheterization
Corticosterone/metabolism
Histamine H1 Antagonists/pharmacology
Histamine H2 Antagonists/pharmacology
Male
Metiamide/pharmacology
Mice
Phenoxypropanolamines
Piperidines/pharmacology
Promethazine/pharmacology
Rats
Rats, Wistar
Thiazoles/pharmacology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Benzothiazoles); 0 (Histamine H1 Antagonists); 0 (Histamine H2 Antagonists); 0 (Phenoxypropanolamines); 0 (Piperidines); 0 (Thiazoles); 3K7670861M (Metiamide); 820484N8I3 (Histamine); 9061-61-4 (Nerve Growth Factor); FF28EJQ494 (Promethazine); M1108XAY01 (zolantidine); W980KJ009P (Corticosterone)
[Em] Entry month:0101
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:010224
[St] Status:MEDLINE

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[PMID]: 10567937
[Au] Autor:Wolff JC; Barr L; Moss P
[Ad] Address:SmithKline Beecham Pharmaceuticals, New Frontiers Science Park North, Third Avenue, Harlow, Essex CM19 5AW, UK. Jean-Claude_Wolff-1@sbphrd.com
[Ti] Title:New ultraviolet signal actuated switching valve for the measurement of low level impurities by liquid chromatography/mass spectrometry.
[So] Source:Rapid Commun Mass Spectrom;13(23):2376-81, 1999.
[Is] ISSN:0951-4198
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:A new ultraviolet (UV) signal actuated switching valve for diverting the main matrix compound to waste, preventing it entering the ion source of the mass spectrometer is described. Sensitivity for trace impurities eluting after the drug substance cimetidine or related compounds could be enhanced by a factor of 4-5. The increase in sensitivity was dependent on the type of ion source which interfaced the mass spectrometer. The benefit of the switching valve was greater with a line of sight type source than with an orthogonal one. The detection limit for a trace compound in a matrix compound was improved by up to a factor of 10 with the line of sight type source but only by a factor of 5 with the orthogonal source.
[Mh] MeSH terms primary: Cimetidine/standards
Drug Contamination
Mass Spectrometry/methods
[Mh] MeSH terms secundary: Cimetidine/chemistry
Metiamide/chemistry
Metiamide/isolation & purification
Molecular Structure
Sensitivity and Specificity
Spectrophotometry, Ultraviolet/methods
Structure-Activity Relationship
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:3K7670861M (Metiamide); 80061L1WGD (Cimetidine)
[Em] Entry month:0001
[Cu] Class update date: 131121
[Lr] Last revision date:131121
[Js] Journal subset:IM
[Da] Date of entry for processing:991124
[St] Status:MEDLINE

  9 / 930 MEDLINE  
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[PMID]: 9972321
[Au] Autor:Ali SA; Peter J; Ali AS
[Ad] Address:Post Graduate Zoology Department, Saifia College of Science and Education, Bhopal, India.
[Ti] Title:Histamine receptors in the skin melanophores of Indian bullfrog Rana tigerina.
[So] Source:Comp Biochem Physiol A Mol Integr Physiol;121(3):229-34, 1998 Nov.
[Is] ISSN:1095-6433
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Histamine and 2-methyl histamine caused dose-dependent aggregation of the integumental melanophores of Rana tigerina both in vitro and in vivo. The aggregating effects were antagonised by mepyramine and metiamide, specific H1 and H2 receptor blockers, respectively. Compound 48/80 and EDTA augmented the melanin-aggregating effects of exogenously applied histamine and 2-methyl histamine in in vivo experiments. 4-Methyl histamine, a specific H2 receptor agonist, dispersed the frog melanophores in in vitro studies, the dispersing effects were blocked by metiamide.
[Mh] MeSH terms primary: Melanophores/metabolism
Ranidae/metabolism
Receptors, Histamine/metabolism
Skin/metabolism
[Mh] MeSH terms secundary: Animals
Edetic Acid/pharmacology
Histamine/pharmacology
Histamine H1 Antagonists/pharmacology
Histamine H2 Antagonists/pharmacology
In Vitro Techniques
Melanins/metabolism
Melanophores/drug effects
Methylhistamines/pharmacology
Metiamide/pharmacology
Pyrilamine/pharmacology
Ranidae/anatomy & histology
Receptors, Histamine/drug effects
Skin/drug effects
Skin Pigmentation/drug effects
Skin Pigmentation/physiology
p-Methoxy-N-methylphenethylamine/pharmacology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Histamine H1 Antagonists); 0 (Histamine H2 Antagonists); 0 (Melanins); 0 (Methylhistamines); 0 (Receptors, Histamine); 3K7670861M (Metiamide); 4091-50-3 (p-Methoxy-N-methylphenethylamine); 54ST71P9EE (4-methylhistamine); 820484N8I3 (Histamine); 9G34HU7RV0 (Edetic Acid); H5DHG2WBHM (2-methylhistamine); HPE317O9TL (Pyrilamine)
[Em] Entry month:9903
[Cu] Class update date: 141120
[Lr] Last revision date:141120
[Js] Journal subset:IM
[Da] Date of entry for processing:990211
[St] Status:MEDLINE

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[PMID]: 9811372
[Au] Autor:Kraly FS; Katz JB; Burchard AE; Case C; Gabriel VA; Lanz TA; Mikkelsen ME; Sokol MB
[Ad] Address:Department of Psychology, Colgate University, Hamilton, NY 13346, USA. skraly@center.colgate.edu
[Ti] Title:H2 histaminergic control of inhibition of eating induced by intragastric NaCl in rats.
[So] Source:Physiol Behav;65(1):105-13, 1998 Aug.
[Is] ISSN:0031-9384
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A role for endogenous histamine and histamine receptor subtypes in mediating the inhibition of eating induced by intragastric (i.g.) hypertonic NaCl was examined in adult male Sprague-Dawley rats surgically equipped with a chronic gastric catheter. The i.g. infusion of 2 mL 900 or 1,800 mOsm/kg of NaCl inhibited: 1) ingestion of pellets in rats eating after 24-h food deprivation; and 2) ingestion of cookies in rats eating without prior deprivation. The H1 receptor antagonists dexbrompheniramine (DXB; 1 mg/kg) and pyrilamine (PYR; 4 mg/kg) did not attenuate the inhibitory effects of i.g. 900 or 1,800 mOsm/kg of NaCl for rats eating pellets and for rats eating cookies. The H2 antagonists cimetidine (CIM; 16 mg/kg) and metiamide (MET; 16 mg/kg) attenuated the inhibitory effects of i.g. 1,800 mOsm/kg of NaCl upon ingestion of cookies, but intracerebroventricular (i.c.v.) infusion (through a chronic indwelling cannula) of 100 microg of CIM did not mimic this effect of intraperitoneal (i.p.) CIM. The i.p. CIM failed to attenuate the inhibition of eating cookies produced by i.p. octapeptide of cholecystokinin (CCK-8; 3 microg/kg). The H3 antagonist thioperamide (TH; 10 mg/kg i.p.) and the H3 agonist R-alpha-methylhistamine (RAM; 3 mg/kg i.p.) did not alter the inhibitory effect of i.g. 1,800 mOsm/kg of NaCl for rats eating cookies. Combined treatments of systemic DXB plus CIM, and DXB plus CIM plus thioperamide (TH) did not reverse the inhibitory effects of i.g. 1,800 mOsm/kg of NaCl upon ingestion of cookies. Finally, i.p. DXB, but not CIM, attenuated the ability of i.g. 900 mOsm/kg of NaCl to increase water intake; conversely, i.p. CIM, but not DXB, attenuated the ability of i.g. 900 mOsm/kg of NaCl to inhibit eating of cookies. These findings demonstrate a double dissociation of effects upon ingestive behavior: H1, but not H2, antagonism attenuates the effect of i.g. hypertonic NaCl on water intake, whereas H2, but not H1, antagonism attenuates the inhibition of eating produced by i.g. hypertonic NaCl. These results demonstrate that different subtypes of peripheral and/or central histamine receptors contribute to different behavioral consequences of postprandial gastrointestinal osmotic loads in rats.
[Mh] MeSH terms primary: Eating/drug effects
Receptors, Histamine H2/physiology
Saline Solution, Hypertonic/pharmacology
[Mh] MeSH terms secundary: Animals
Drinking/drug effects
Histamine/physiology
Histamine Antagonists/pharmacology
Histamine H1 Antagonists/pharmacology
Histamine H2 Antagonists/pharmacology
Injections, Intraperitoneal
Injections, Intraventricular
Intubation, Gastrointestinal
Male
Osmolar Concentration
Rats
Rats, Sprague-Dawley
Receptors, Histamine H1/drug effects
Receptors, Histamine H1/physiology
Receptors, Histamine H2/drug effects
Receptors, Histamine H3/drug effects
Receptors, Histamine H3/physiology
Saline Solution, Hypertonic/administration & dosage
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Name of substance:0 (Histamine Antagonists); 0 (Histamine H1 Antagonists); 0 (Histamine H2 Antagonists); 0 (Receptors, Histamine H1); 0 (Receptors, Histamine H2); 0 (Receptors, Histamine H3); 0 (Saline Solution, Hypertonic); 820484N8I3 (Histamine)
[Em] Entry month:9901
[Cu] Class update date: 131121
[Lr] Last revision date:131121
[Js] Journal subset:IM
[Da] Date of entry for processing:981112
[St] Status:MEDLINE


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