0000000000064374

AUTHOR

Bernard Muller

showing 2 related works from this author

Glycyrrhetinic Acid Reverses the Lipopolysaccharide-Induced Hypocontractility to Noradrenaline in Rat Aorta: Implications to Septic Shock

2014

Abstract.: Septic shock and associated vascular hyporeactivity to vasoconstrictor agonists remain a major problem of critical care medicine. Here we report that glycyrrhetinic acid (GA), the active component of licorice, effectively restores vascular contractility in the model of lipopolysaccharide (LPS)-treated rat aorta. GA was as effective as the NO synthase inhibitor NG-nitroarginine methylester. GA did not affect the vascular NO levels (measured by EPR spin trapping) and relaxations to l-arginine in LPS-treated rings as well as relaxation to S-nitroso-Nacetylpenicillamine in control rings. Thus, GA may represent an interesting alternative to NO synthase inhibitors in sepsis-associated …

LipopolysaccharidesMaleLipopolysaccharideArgininePharmacologychemistry.chemical_compoundNorepinephrinemedicine.arteryActive componentNo synthaseGlycyrrhizaMedicineAnimalsEnzyme InhibitorsRats WistarAortaPharmacologyVascular contractilityAortabusiness.industrySeptic shocklcsh:RM1-950medicine.diseaseShock SepticEpr spin trappinglcsh:Therapeutics. PharmacologychemistryBiochemistryVasoconstrictionMolecular MedicineGlycyrrhetinic AcidNitric Oxide SynthasebusinessPhytotherapyJournal of Pharmacological Sciences
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Biopterin metabolism and eNOS expression during hypoxic pulmonary hypertension in mice.

2013

International audience; Tetrahydrobiopterin (BH$_4$), which fosters the formation of and stabilizes endothelial NO synthase (eNOS) as an active dimer, tightly regulates eNOS coupling / uncoupling. Moreover, studies conducted in genetically-modified models demonstrate that BH$_4$ pulmonary deficiency is a key determinant in the pathogenesis of pulmonary hypertension. The present study thus investigates biopterin metabolism and eNOS expression, as well as the effect of sepiapterin (a precursor of BH$_4$) and eNOS gene deletion, in a mice model of hypoxic pulmonary hypertension. In lungs, chronic hypoxia increased BH$_4$ levels and eNOS expression, without modifying dihydrobiopterin (BH$_2$, t…

medicine.medical_specialtySepiapterinNitric Oxide Synthase Type III[SDV]Life Sciences [q-bio]Hypertension PulmonaryBiopterinlcsh:Medicine[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineEnosRight ventricular hypertrophyDihydrobiopterinInternal medicinemedicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]AnimalsHypoxialcsh:Science[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biology0303 health sciencesMultidisciplinarybiologylcsh:RHypoxia (medical)biology.organism_classificationmedicine.diseasePulmonary hypertensionBiopterin[SDV] Life Sciences [q-bio]Disease Models AnimalTetrahydrofolate DehydrogenaseEndocrinologychemistryVentricular pressurelcsh:Qmedicine.symptomResearch ArticlePLoS ONE
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