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-martinez

subject

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.drug

description

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.

10.1111/j.2042-7158.1991.tb03198.xhttps://pubmed.ncbi.nlm.nih.gov/1687588