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Evidence has shown that the changes in placental NO metabolism are unlikely to be the main cause of placental lesions, that the higher level of circulating NO metabolites may be to compensate for the vasoconstrictor effect of preeclampsia, and that the vascular system of patients with preeclampsia may also have some degree of desensitization or resistance to the effects of NO (74)

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In parallel, many of these agents induce reactive oxygen species (ROS) and mitochondrial dysfunction, which amplify epithelial damage by promoting apoptosis, inflammatory signaling, and loss of barrier integrity (Figure 2) (42)

doi: 10.1124/dmd.115.065276, 100