Search results for "P.O.S"

showing 10 items of 5765 documents

Characterization of choline efflux from the perfused heart at rest and after muscarine receptor activation.

1986

The resting efflux of choline from perfused chicken hearts varied from 0.4 to 2.6 nmol/g min, but was constant for at least 80 min in the individual experiments. The rate of choline efflux was found to be equal to the rate of choline formation in the heart, which, from the following reasons, was essentially due to hydrolysis of choline phospholipids. Cardiac content of choline phospholipids (7,200 nmol/g) was much higher than that of acetylcholine (5.5 nmol/g). Resting release of acetylcholine was 0.016 nmol/g min and, after inhibition of cholinesterase, only about 0.1 nmol/g min. Resting efflux of choline was reduced by mepacrine, a phospholipase A2 inhibitor, by perfusion with a Ca2+-free…

medicine.medical_specialtyTime FactorsOleic AcidsIn Vitro TechniquesCholinechemistry.chemical_compoundInternal medicinemedicineCholineAnimalsMagnesiumPhospholipidsCholinesterasePharmacologyMuscarinebiologyMyocardiumGeneral MedicineIsolated heartMyocardial ContractionReceptors MuscarinicPerfusionEndocrinologychemistryParasympathomimeticsQuinacrinebiology.proteinCalciumEffluxCholine formationReceptor activationChickensAcetylcholinemedicine.drugOleic AcidNaunyn-Schmiedeberg's archives of pharmacology
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Addition of NMDA-receptor antagonist MK801 during oxygen/glucose deprivation moderately attenuates the upregulation of glucose uptake after subsequen…

2011

During stroke the blood–brain barrier (BBB) is damaged which can result in vasogenic brain edema and inflammation. The reduced blood supply leads to decreased delivery of oxygen and glucose to affected areas of the brain. Oxygen and glucose deprivation (OGD) can cause upregulation of glucose uptake of brain endothelial cells. In this letter, we investigated the influence of MK801, a non-competitive inhibitor of the NMDA-receptor, on the regulation of the glucose uptake and of the main glucose transporters glut1 and sglt1 in murine BBB cell line cerebEND during OGD. mRNA expression of glut1 was upregulated 68.7- fold after 6 h OGD, which was significantly reduced by 10 μM MK801 to 28.9-fold.…

medicine.medical_specialtyTime FactorsSchlaganfallNMDA-RezeptorGlucose uptakeNMDA-AntagonistInflammationCarbohydrate metabolismTritiumBlood–brain barrierReceptors N-Methyl-D-AspartateMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationInternal medicinemedicineBlut-Hirn-SchrankeAnimalsddc:610RNA MessengerHypoxia030304 developmental biology0303 health sciencesDose-Response Relationship DrugbiologyGeneral NeuroscienceGlucosetransportproteineGlucose transporterBrainEndothelial CellsUp-RegulationOxygencarbohydrates (lipids)Glucosemedicine.anatomical_structureEndocrinologynervous systembiology.proteinNMDA receptorGLUT1Dizocilpine Maleatemedicine.symptomExcitatory Amino Acid Antagonists030217 neurology & neurosurgeryNeuroscience Letters
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Localization of the bradykinin B2 receptor in uterus, bladder and Madin-Darby canine kidney cells

1997

Kinins are biologically active peptides that act through specific receptors, B1 and B2. Here we describe the localization of the bradykinin B2 receptor in Madin-Darby canine kidney cells and in the uterus and urinary bladder of rat or human origin. We discuss the suitability of anti-peptide antibodies to assess the tissue distribution of bradykinin B2 receptors.

medicine.medical_specialtyTissue FixationReceptor Bradykinin B2Urinary BladderUterusBradykininKidneyRadioligand Assaychemistry.chemical_compoundDogsAntibody SpecificityInternal medicineTumor Cells CulturedmedicineAnimalsHumansTissue DistributionReceptorPharmacologyKidneyParaffin EmbeddingUrinary bladderbiologyurogenital systemReceptors BradykininUterusImmunohistochemistryRadioligand AssayRatsmedicine.anatomical_structureEndocrinologyMicroscopy Fluorescencechemistrybiology.proteinCancer researchAutoradiographyImmunohistochemistryElectrophoresis Polyacrylamide GelFemaleAntibodyCell DivisionImmunopharmacology
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Regulation of PTHrP and PTH/PTHrP receptor by extracellular Ca2+ concentration and hormones in the breast cancer cell line 8701-BC.

2000

AbstractIt was previously reported that 8701-BC breast tumour cells express the gene for parathyroid hormonerelated peptide (PTHrP) and PTH/PTHrP receptor (PTHrPR) and release immunoreactive PTHrP (iPTHrP) into the extracellular medium. Since the regulation of PTHrP and PTHrPR by breast cancer cells has been poorly investigated so far, we have chosen the 8701- BC cell line as a model system to investigate whether alterations in the extracellular Ca[2+] concentration ([Ca[2+]]) and treatment with some wellknown differentiation agents for breast cells, such as dimethyl sulfoxide, hydrocortisone, progesterone, prolactin, alltrans retinoic acid and transforming growth factorβ1 might (i) modulat…

medicine.medical_specialtyTranscription GeneticRNA SplicingClinical BiochemistryRetinoic acidCodon InitiatorBreast NeoplasmsTretinoinBiochemistrychemistry.chemical_compoundTranscription (biology)Transforming Growth Factor betaInternal medicinemedicineExtracellularTumor Cells CulturedHumansProtein IsoformsRNA MessengerPromoter Regions GeneticMolecular BiologyGeneChemistryParathyroid Hormone-Related ProteinProteinsProlactinHormonesNeoplasm ProteinsEndocrinologyGene Expression RegulationCell cultureRNA splicingReceptors Parathyroid HormoneCalciumExtracellular Spacehormones hormone substitutes and hormone antagonistsHormoneBiological chemistry
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Proliferative effect of acetylcholine on rat trachea epithelial cells is mediated by nicotinic receptors and muscarinic receptors of the M1-subtype.

2003

Acetylcholine (ACh), synthesized in mammalian non-neuronal cells such as epithelial cells of the airways, digestive tract and skin, is involved in the regulation of basic cell functions (so-called non-neuronal cholinergic system). In the present experiments rat trachea epithelial cells have been cultured to study the proliferative effect of applied ACh by [3H]thymidine incorporation. ACh (exposure time 24 h) caused a concentration-dependent increase in cell proliferation with a doubling of the [3H]thymidine incorporation at a concentration of 0.1 microM. This effect was partly reduced by 30 microM tubocurarine and completely abolished by the additional application of 1 microM atropine. The …

medicine.medical_specialtyTubocurarineMuscarinic AntagonistsNicotinic AntagonistsBiologyReceptors NicotinicGeneral Biochemistry Genetics and Molecular BiologyRats Sprague-DawleyInternal medicineMuscarinic acetylcholine receptormedicineMuscarinic acetylcholine receptor M4AnimalsGeneral Pharmacology Toxicology and PharmaceuticsNicotinic AntagonistReceptor Muscarinic M1Muscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Epithelial CellsGeneral MedicineMolecular biologyPirenzepineReceptors MuscarinicAcetylcholineRatsTracheaAtropineEndocrinologyAcetylcholineCell Divisionmedicine.drugThymidineLife sciences
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Progestogens stimulate prostacyclin production by human endothelial cells.

2005

BACKGROUND: The effects of progestogens on endothelial physiology are poorly studied. Prostacyclin is a potent vasodilator synthesized by two isoforms of cyclooxygenase (COX) in endothelium. We examined the effects of two clinically used progestogens, progesterone and medroxyprogesterone acetate (MPA), on prostacyclin production by cultured human umbilical vein endothelial cells (HUVEC) and the possible role of progesterone receptors and both COX enzymes. METHODS: Cells were exposed to 1-100 nmol/l of either progesterone or MPA and prostacyclin production was measured in culture medium. RESULTS: Both progestogens significantly increased prostacyclin release in a time- and dose-dependent man…

medicine.medical_specialtyUmbilical VeinsEndotheliumProstacyclinMedroxyprogesterone AcetateUmbilical veinInternal medicineProgesterone receptormedicineMedroxyprogesterone acetateHumansCyclooxygenase InhibitorsReceptorCells CulturedNitrobenzenesProgesteroneSulfonamidesbiologyCyclooxygenase 2 InhibitorsDose-Response Relationship DrugEstradiolRehabilitationObstetrics and GynecologyEndothelial CellsMembrane ProteinsEpoprostenolEndothelial stem cellMifepristoneEndocrinologymedicine.anatomical_structureReproductive MedicineCyclooxygenase 2Prostaglandin-Endoperoxide Synthasescardiovascular systembiology.proteinCyclooxygenase 1PyrazolesCyclooxygenaseEndothelium VascularProgestinsReceptors Progesteronemedicine.drugHuman reproduction (Oxford, England)
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Psoas hitch and Boari flap ureteroneocystostomy

2013

medicine.medical_specialtyUreter surgerybusiness.industryUrologyPsoas hitchMedicineBoari flapAnastomosisbusinessUreteric reimplantationSurgeryBJU International
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The pharmacological rationale for combining muscarinic receptor antagonists and beta-adrenoceptor agonists in the treatment of airway and bladder dis…

2014

Highlights • Muscarinic receptors increase smooth muscle tone in airways and urinary bladder. • β-Adrenoceptors relax smooth muscle tone and oppose muscarinic contraction. • Opposition involves transmitter release, signal transduction and receptor expression. • This supports the combined use of muscarinic antagonists and β-adrenoceptor agonists.

medicine.medical_specialtyUrologyDiseaseMuscarinic AntagonistsPharmacologyArticleβ adrenoceptorchemistry.chemical_compoundInternal medicineReceptors Adrenergic betaMuscarinic acetylcholine receptorDrug DiscoveryMuscarinic acetylcholine receptor M4RAT URINARY-BLADDERMedicineAnimalsHumansCyclic adenosine monophosphateADRENERGIC RELAXATIONLung Diseases ObstructivePROTEIN-KINASE-CReceptorTRACHEAL SMOOTH-MUSCLEPharmacologybusiness.industryUrinary Bladder DiseasesMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2ACETYLCHOLINE-RELEASEAdrenergic beta-Agonistsmedicine.diseaseReceptors MuscarinicEndocrinologyNONNEURONAL CHOLINERGIC SYSTEMchemistryGUINEA-PIG TRACHEADrug Therapy CombinationCYCLIC ADENOSINE-MONOPHOSPHATECA2+-ACTIVATED K+ CHANNELAirwaybusinessUrinary bladder diseaseAUTORADIOGRAPHIC VISUALIZATIONAcetylcholinemedicine.drug
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Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis.

2014

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing…

medicine.medical_specialtyVascular smooth musclePhysiologyCell Survivalmedicine.medical_treatmentMyocytes Smooth MuscleCX3C Chemokine Receptor 1InflammationMice TransgenicBiologyMuscle Smooth VascularInsulin resistanceApolipoproteins EPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayCells CulturedMice KnockoutChemokine CX3CL1Insulinmedicine.diseaseAtherosclerosisIRS2Mice Inbred C57BLAtheromaEndocrinologyDiabetes Mellitus Type 2cardiovascular systemReceptors Chemokinemedicine.symptomInsulin ResistanceCardiology and Cardiovascular MedicineSignal TransductionCardiovascular research
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Dopaminergic modulation of evoked vasopressin release from the isolated neurohypophysis of the rat

1982

1. Neurointermediate lobes of rat pituitaries were incubated in Locke or Krebs solution, and the vasopressin released into the medium was assayed on the blood pressure of the pithed rat or by a radioimmunological procedure. Release of vasopressin over resting levels was evoked either by incubation with 60 mM KCl (high K) solution or by electrical stimulation of the pituitary stalk. Two different kinds of electrical stimulation were carried out. Procedure A (1 ms, 10 Hz, 5 times for 1 min within 10 min) induced a vasopressin overflow which was greatly calcium-dependent but only insignificantly sensitive to tetrodotoxin (TTX). Procedure B (0.2 ms, 15 Hz, 10 s trains with 10 s intervals for 10…

medicine.medical_specialtyVasopressinApomorphineVasopressinsDopamineStimulationTetrodotoxinIn Vitro TechniquesReceptors DopaminePituitary Gland PosteriorDopamineInternal medicinemedicineAnimalsBromocriptineEndogenous opioidPharmacologyNaloxoneChemistryDopaminergicRats Inbred StrainsGeneral MedicineElectric StimulationRatsFlupenthixolApomorphineEndocrinologyDopamine receptorFemaleEndorphinsSulpirideSulpiridemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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