Exposure to NO synthase inhibitor (N-nitro-L-arginine methyl ester) decreases eNOS production of NO, increases vasoconstriction and hypertension, and decreases survival of these mice, while pretreatment with ET(A) receptor antagonist (darusentan) improves survival, indicating that increased NO production in these mice suppresses the adverse effects associated with increased ET-1 (Quaschning et al., 2003). This evidence concerns the gene EDN1 and Hypertension.