Hypoxic pulmonary vasoconstriction is enhanced by inhibition of the synthesis of an endothelium derived relaxing factor

Inhibition of the synthesis of endothelium derived relaxing factor by N^G-monomethyl-L-arginine, a competitive inhibitor of the synthesis of nitric oxide from L-arginine, enhances hypoxic pulmonary vasoconstriction in pulmonary artery rings and isolated, Krebs albumin perfused rat lungs. L-arginine rapidly reduces hypoxic vasoconstriction, particularly in lungs treated with N^G-monomethyl-L-arginine. Following administration of N^G-monomethyl-L-arginine, bradykinin-induced vasodilation is inhibited (p<0.01) and a bradykinin-induced vasoconstriction develops (p<0.001). N^G-monomethyl-L-arginine does not significantly diminish acetylcholine-induced vasodilatation in the isolated lung. N^G-monomethyl-L-arginine causes an endothelium-dependent vasoconstriction in pulmonary artery rings.