Biased activation of soluble guanylyl cyclase by quinones causes contractions of isolated arteries: Role of NADPH: quinone oxidoreductase-1

Abstract

Background Previous experiments in isolated arteries indicate that quinones, including thymoquinone (a para-quinone) and β-lapachone [an ortho-quinone and high-affinity substrate of NADPH:quinone oxidoreductase-1 (NQO-1)], causes augmentations of contraction. The augmentation depends on the activation of soluble guanylyl cyclase (sGC) to generate cyclic inosine monophosphate (cIMP) rather than the canonical cyclic guanosine monophosphate (cGMP). The present study aims to identify cellular target of the quinones in mediating the biased activation of sGC.