The mechanisms of vasorelaxation elicited by N(omega)-hydroxy-L-arginine (L-NOHA) and other compounds bearing a C=NOH function and the structural determinants governing this effect were investigated in rat aorta. L-NOHA, formamidoxime, five aromatic monosubstituted amidoximes, and one aromatic monosubstituted ketoxime elicited relaxation in endothelium-denuded rings. N-Hydroxyguanidine and substituted N-hydroxyguanidines were markedly less active.
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