L-arginine restores endothelium-dependent relaxation in pulmonary circulation of chronically hypoxic rats.

摘要: We investigated whether loss of endothelial-derived relaxing factor (EDRF) activity in the pulmonary vessels chronically hypoxic rats could be restored by pretreatment with L-arginine. measured vasodilation to acetylcholine (ACh), calcium ionophore A23187, or linsidomine (Sin-1) under conditions increased vascular tone induced U-46619 (50 pmol/min), as well vasoconstriction endothelin-1 (ET) isolated lungs pretreated meclofenamate (3 microM). In from normoxic (N) rats, vitro L- D-arginine (10(-3) M) did not alter endothelium-dependent agents ACh (10(-9)-10(-6) and A23187 (10(-9)-10(-7) M), but NG-monomethyl-L-arginine completely abolished it. exposed 3 wk hypoxia (H), was fully after L-arginine N alpha-benzoyl-L-arginine (5 x 10(-5) remained D-arginine, L-citrulline, L-ornithine, L-argininosuccinic acid. vivo H (300 mg/kg iv) 30 min before isolating lung also A23187. Vasodilation endothelium-independent agent Sin-1 similar both groups altered attenuated pressor response ET pmol) rat had no effect rats. Our results demonstrate that EDRF associated hypertension may reversed supplying