Search results for "Cyclic GMP"

showing 10 items of 99 documents

Effect of beta-N-oxalylamino-L-alanine on cerebellar cGMP level in vivo.

1993

Beta-N-oxalylamino-L-alanine (BOAA), a non-protein amino acid present in the seeds of Lathyrus Sativus (LS), is one of several neuroactive glutamate analogs reported to stimulate excitatory receptors and, in high concentrations, cause neuronal degeneration. In the present study, the in vivo acute effects of synthetic BOAA and LS seed extract were investigated on rat cerebellar cyclic GMP following intraperitoneal (10-100 mg/kg) or oral (100 mg/kg) administration of subconvulsive doses of toxin. Furthermore, the BOAA content in LS seeds and in the cerebellum of injected rats was determined by high performance liquid chromatograph analysis. A dose- and time-dependent increase of cerebellar cy…

Malemedicine.medical_specialtyCerebellumAdministration OralStimulationBiologyBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundKynurenic acidIn vivoInternal medicineCerebellummedicineNeurotoxinAnimalsRats WistarCyclic guanosine monophosphateCyclic GMPChromatography High Pressure LiquidLathyrismGlutamate receptorAmino Acids DiaminoGeneral Medicinemedicine.diseaseRatsEndocrinologymedicine.anatomical_structurechemistrybeta-AlanineInjections IntraperitonealNeurochemical research
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Chronic Therapy With Isosorbide-5-Mononitrate Causes Endothelial Dysfunction, Oxidative Stress and a Marked Increase in Vascular Endothelin-1 Express…

2011

Aims Isosorbide-5-mononitrate (ISMN) is one of the most frequently used compounds in the treatment of coronary artery disease predominantly in the USA. However, ISMN was reported to induce endothelial dysfunction, which was corrected by vitamin C pointing to a crucial role of reactive oxygen species (ROS) in causing this phenomenon. We sought to elucidate the mechanism how ISMN causes endothelial dysfunction and oxidative stress in vascular tissue. Methods and results Male Wistar rats ( n = 69 in total) were treated with ISMN (75 mg/kg/day) or placebo for 7 days. Endothelin (ET) expression was determined by immunohistochemistry in aortic sections. Isosorbide-5-mononitrate infusion caused si…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIIsosorbide DinitratePharmacologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesEnosInternal medicinePhysiology (medical)medicineAnimalsNitric Oxide DonorsEnzyme InhibitorsRats WistarEndothelial dysfunctionCyclic GMPAortaMice KnockoutNADPH oxidaseEndothelin-1biologybusiness.industryNADPH Oxidasesmedicine.diseasebiology.organism_classificationEndothelin 1BosentanRatsNitric oxide synthaseEndothelial stem cellOxidative StressNG-Nitroarginine Methyl EsterEndocrinologychemistryApocyninbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineEndothelin receptorbusinessOxidative stressSignal Transductionmedicine.drugFree Radical Biology and Medicine
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Cardiac effects of isoliquiritigenin

1997

The effects of isoliquiritigenin on force of contraction (Fc), L-type Ca2+ current (I(Ca)) and intracellular Ca2+ concentration ([Ca2+]i) were investigated in rat ventricular heart muscle. Isoliquiritigenin increased Fc and I(Ca) and, after longer exposure times, resting tension and [Ca2+]i. The effect of isoliquiritigenin (100 microM) on I(Ca) was diminished by Rp-cAMPS (30 microM). 1H-[1,2,4]oxa- diazolo[4,3-a]quinoxalin-1-one (50 microM) did not influence the effects of isoliquiritigenin on Fc and I(Ca). The positive inotropic effects of isoprenaline and forskolin, but not of 3-isobutyl-1-methylxanthine, were potentiated by isoliquiritigenin (100 microM). In the presence of milrinone (10…

Malemedicine.medical_specialtyPatch-Clamp TechniquesFura-2In Vitro TechniquesMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundChalconeChalconesAldehyde ReductaseInternal medicineIsoprenalinemedicineAnimalsDrug InteractionsEnzyme InhibitorsCyclic GMPPharmacologyPlants MedicinalForskolinMyocardiumPhosphodiesteraseHeartCyclic AMP-Dependent Protein KinasesMyocardial ContractionRatsElectrophysiologyEndocrinologychemistryGuanylate CyclaseMilrinoneCalciumFemalemedicine.symptomSoluble guanylyl cyclaseIsoliquiritigeninMuscle contractionmedicine.drugEuropean Journal of Pharmacology
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Protein synthesis and cyclic GMP content in rat cardiac muscle after swimming exercise

1988

Rats were exercised for 6 h by swimming. Phenylalanine incorporation into myocardial proteins was increased when 2 h had elapsed after the termination of exercise. Cyclic GMP concentration did not change during the experiment, which indicates that cyclic GMP does not act directly as a trigger of myocardial protein synthesis in volume overload.

Malemedicine.medical_specialtySwimming exercisePhenylalaninePhysical ExertionVolume overloadPhenylalaninePhysical exerciseCellular and Molecular NeuroscienceCyclic gmpInternal medicinemedicineProtein biosynthesisAnimalsCyclic GMPMolecular BiologySwimmingPharmacologybusiness.industryMyocardiumCardiac muscleRats Inbred StrainsCell BiologyRatsmedicine.anatomical_structureEndocrinologyProtein BiosynthesisCirculatory systemMolecular MedicinebusinessExperientia
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Biphasic 24-Hour Variations in Cyclic GMP Accumulation in the Rat Pineal Gland Are Due to Corresponding Changes in the Activity of Cytosolic and Part…

2006

Various parameters of the rat pineal gland display a 24-h rhythm. However, nothing is known about possible 24-h variations in cyclic GMP (cGMP) metabolism. In the present study, 24-h variations in pineal gland cGMP accumulation were investigated by determining the increase in cGMP level with and without inhibitors of phosphodiesterase at different time points over a light/dark cycle (12/12 h). Furthermore, the activity of guanylate cyclase (GC) was determined under substrate-saturated conditions regarding the cytosolic and particulate forms of the enzyme. It has been found that cGMP accumulation and GC activity display biphasic 24-h variations with two peaks--one approximately 7 h after lig…

Malemedicine.medical_specialtyTime FactorsBiologyArginineNitric OxidePineal GlandBiochemistryNitric oxideRats Sprague-DawleyCellular and Molecular NeurosciencePineal glandchemistry.chemical_compoundCytosolInternal medicinemedicineAnimalsCircadian rhythmCyclic GMPchemistry.chemical_classificationomega-N-MethylargininePhosphodiesteraseMetabolismCircadian RhythmRatsEnzyme ActivationCytosolEnzymeEndocrinologymedicine.anatomical_structurechemistryBiochemistryGuanylate CyclaseEndocrine glandJournal of Neurochemistry
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Microvascular effects of the inhibition of dipeptidylpeptidase IV by linagliptin in nondiabetic hypertensive patients

2015

Recent studies suggest vascular benefits of dipeptidylpeptidase IV (DPP-IV) inhibition in patients with diabetes mellitus. Only little is known about potential vascular effects of DPP-IV inhibitors in nondiabetic individuals. The aim of this study was to investigate the effect of DPP-IV inhibition in a nondiabetic hypertensive population.This was a double-blinded, randomized, placebo-controlled, mechanistic study, comparing microvascular effects of the DPP-IV inhibitor linagliptin with placebo in nondiabetic individuals with a history of arterial hypertension. Twenty-one patients received 5 mg linagliptin (5 women; age 67.6 ± 6.0 years; mean ± SD), whereas 22 patients were randomized to pla…

Malemedicine.medical_specialtyanimal structuresPhysiologyMEDLINELinagliptin030209 endocrinology & metabolism030204 cardiovascular system & hematologyArginineLinagliptinlaw.inventionTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineDouble-Blind MethodRandomized controlled triallawDiabetes mellitusInternal medicineInternal MedicinemedicineHumansArterial PressureIn patientCystatin CCyclic GMPDipeptidylpeptidase ivAgedGlycated HemoglobinDipeptidyl-Peptidase IV Inhibitorsbusiness.industryRetinal VesselsMiddle Agedmedicine.diseaseC-Reactive ProteinEndocrinologyRegional Blood FlowHypertensionMicrovesselsFemaleCardiology and Cardiovascular Medicinebusinessmedicine.drugJournal of Hypertension
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Nebivolol inhibits superoxide formation by NADPH oxidase and endothelial dysfunction in angiotensin II-treated rats.

2006

Nebivolol is a β 1 -receptor antagonist with vasodilator and antioxidant properties. Because the vascular NADPH oxidase is an important superoxide source, we studied the effect of nebivolol on endothelial function and NADPH oxidase activity and expression in the well-characterized model of angiotensin II–induced hypertension. Angiotensin II infusion (1 mg/kg per day for 7 days) caused endothelial dysfunction in male Wistar rats and increased vascular superoxide as detected by lucigenin-derived chemiluminescence, as well as dihydroethidine staining. Vascular NADPH oxidase activity, as well as expression at the mRNA and protein level, were markedly upregulated, as well as NOS III uncoupled, …

Malerac1 GTP-Binding Proteinmedicine.medical_specialtyLuminescenceEndotheliumNitric Oxide Synthase Type IIIAdrenergic beta-AntagonistsNitric OxideFluorescenceCell LineNebivololchemistry.chemical_compoundHemoglobinsSuperoxidesInternal medicineInternal MedicinemedicineAnimalsHumansBenzopyransRats WistarCyclic GMPNitritesOxidase testNADPH oxidaseLuminescent AgentsbiologyChemistrySuperoxideAngiotensin IIMyocardiumNADPH OxidasesDicarbethoxydihydrocollidinePhosphoproteinsAngiotensin IINebivololRatsNitric oxide synthasemedicine.anatomical_structureEndocrinologyEthanolaminesNOX1biology.proteinAcridinesBlood VesselsLuminolEndothelium Vascularmedicine.drugSignal TransductionHypertension (Dallas, Tex. : 1979)
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Evidence for a relationship between mitochondrial Complex I activity and mitochondrial aldehyde dehydrogenase during nitroglycerin tolerance: effects…

2012

The medical use of nitroglycerin (GTN) is limited by patient tolerance. The present study evaluated the role of mitochondrial Complex I in GIN biotransformation and the therapeutic effect of mitochondrial antioxidants. The development of GIN tolerance (in rat and human vessels) produced a decrease in mitochondrial 02 consumption. Co-incubation with the mitochondria-targeted antioxidant mitoquinone (MQ 10(-6) mol/L) or with glutathione ester (GEE, 10(-4) mol/L) blocked GTN tolerance and the effects of GTN on mitochondrial respiration and aldehyde dehydrogenase 2 (ALDH-2) activity. Biotransformation of GTN depended on the mitochondria being functionally active, particularly mitochondrial Comp…

Mitochondrial ROSMaleAntioxidantmedicine.medical_treatmentAldehyde dehydrogenaseMitochondrionmedicine.disease_causeBiochemistryAntioxidantsRats Sprague-Dawleychemistry.chemical_compoundMiceNitroglycerinCyclic GMPAortaBiotransformationbiologyDrug ToleranceGlutathioneMitochondriaVasodilationBiochemistrycardiovascular systemAntioxidantcirculatory and respiratory physiologyBiophysicsIn Vitro TechniquesALDH-2Nitric oxideCell LineOxygen ConsumptionRotenoneRespirationmedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansElectron Transport Complex IDose-Response Relationship DrugNitric oxideGlutathioneCell BiologyAldehyde DehydrogenaseRatschemistryOxidative stressMutationbiology.proteinReactive Oxygen SpeciesOxidative stressBiochimica et biophysica acta
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Reciprocal regulation of endothelial nitric-oxide synthase and NADPH oxidase by betulinic acid in human endothelial cells.

2007

Nitric oxide (NO) produced by endothelial NO synthase (eNOS) is a protective principle in the vasculature. Many cardiovascular diseases are associated with reduced NO bioactivity and eNOS uncoupling due to oxidative stress. Compounds that reverse eNOS uncoupling and increase eNOS expression are of therapeutic interest. Zizyphi Spinosi semen (ZSS) is one of the most widely used traditional Chinese herbs with protective effects on the cardiovascular system. In human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells, an extract of ZSS increased eNOS promoter activity, eNOS mRNA and protein expression, and NO production in a concentration- and time-dependent manner. Maj…

Nitric Oxide Synthase Type IIIBlotting Westernmedicine.disease_causeNitric OxideGene Expression Regulation EnzymologicNitric oxidechemistry.chemical_compoundEnosBetulinic acidmedicineHumansNitric Oxide DonorsEnzyme InhibitorsBetulinic AcidCyclic GMPCells CulturedPharmacologyNADPH oxidaseBetulinbiologyDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionNOX4AcetophenonesEndothelial CellsNADPH OxidasesZiziphusSaponinsbiology.organism_classificationTriterpenesNG-Nitroarginine Methyl EsterchemistryBiochemistryNADPH Oxidase 4biology.proteinMolecular MedicineSpermineP22phoxPentacyclic TriterpenesReactive Oxygen SpeciesOxidative stressDrugs Chinese HerbalThe Journal of pharmacology and experimental therapeutics
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Postsynaptic NO/cGMP Increases NMDA Receptor Currents via Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels in the Hippocampus

2013

The nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling cascade participates in the modulation of synaptic transmission. The effects of NO are mediated by the NO-sensitive cGMP-forming guanylyl cyclases (NO-GCs), which exist in 2 isoforms with indistinguishable regulatory properties. The lack of long-term potentiation (LTP) in knock-out (KO) mice deficient in either one of the NO-GC isoforms indicates the contribution of both NO-GCs to LTP. Recently, we showed that the NO-GC1 isoform is located presynaptically in glutamatergic neurons and increases the glutamate release via hyperpolarization-activated cyclic nucleotide (HCN)-gated channels in the hippocampus. Electrophysiologi…

Patch-Clamp TechniquesCognitive NeuroscienceLong-Term PotentiationIn Vitro TechniquesNeurotransmissionNitric OxideReceptors N-Methyl-D-AspartateMiceCellular and Molecular Neurosciencechemistry.chemical_compoundCyclic nucleotidePostsynaptic potentialHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsHCN channelAnimalsAnesthetics LocalCA1 Region HippocampalCyclic GMPCyclic guanosine monophosphateMice KnockoutNeuronsbiologyLidocaineTetraethylammoniumLong-term potentiationHyperpolarization (biology)Electric StimulationPyrimidinesAnimals Newbornnervous systemchemistryGuanylate CyclaseBiophysicsbiology.proteinNMDA receptorExcitatory Amino Acid AntagonistsNeuroscienceCerebral Cortex
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