For instance, we understand that in the cases of preeclampsia with low NO production (low NO2/NO3 levels) the alterations are related with a deficiency in the substrate L-arginine, a deficit in the cofactors that are needed for a normal activity of the eNOS, such as ionic calcium and BH4, build-up of the endogenous inhibitor of eNOS, the asymmetric dimethylarginine (ADMA), or by the presence of polymorphic alterations of the eNOS that result in a lower enzymatic activity (Serrano et al., 2004; Lopez-Jaramillo et al., 2008a). This evidence concerns the gene NOS3 and preeclampsia.