6533b872fe1ef96bd12d2e7b
RESEARCH PRODUCT
NG-monomethyl-L-arginine and NG-nitro-L-arginine inhibit endothelium-dependent relaxations in human isolated omental arteries.
J.m. VilaJuan V. EspluguesBlas FlorMartin AldasoroM. A. Martínez-cuestaSalvador LluchM C Martinez-martinezsubject
inorganic chemicalsAdultMalemedicine.medical_specialtyEndotheliumArginineMuscle RelaxationPharmaceutical ScienceVasodilationIn Vitro TechniquesArginineNitric OxideMuscle Smooth VascularNitric oxidechemistry.chemical_compoundInternal medicinemedicineHumansAgedPharmacologyomega-N-MethylarginineAnatomyArteriesMiddle AgedAcetylcholineEndocrinologymedicine.anatomical_structureNG-Nitroarginine Methyl EsterchemistryRegional Blood Flowcardiovascular systemOmega-N-MethylarginineFemaleSodium nitroprussideEndothelium VascularOmentumAcetylcholineBlood vesselmedicine.drugdescription
Abstract The L-arginine analogues NG-monomethyl-l-arginine (l-NMMA, 10−4 m) and NG-nitro-L-arginine methyl ester (l-NAME, 10−4 m), which specifically inhibit the synthesis of nitric oxide from l-arginine, significantly reduced acetylcholine-induced endothelium-dependent relaxations in rings of human omental arteries. The inhibitory potency of l-NMMA and l-NAME was similar. Addition of l-NMMA or l-NAME to the organ bath did not induce any significant changes in the resting tension of the tissues. The effects of l-NMMA were reversed by l-arginine (3 × 10−4 m). The l-NMMA enantiomer, d-NMMA (10−4 m), did not influence either the basal tone of the preparation or the relaxing effects of acetylcholine. Arterial relaxations induced by sodium nitroprusside (10−6 m) were not influenced by incubation with l-NMMA or l-NAME. These results suggest that endothelium-dependent relaxations in human omental arteries are mediated by the endogenous and substrate-specific generation of nitric oxide from l-arginine.
year | journal | country | edition | language |
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1991-12-01 | The Journal of pharmacy and pharmacology |