Endothelial dysfunction, resulting from increased reactive oxygen species (ROS; e.g., superoxide and peroxynitrite, the reactive nitrogen intermediate), reduced bioavailable NO, or impaired NO-induced activation of oxidized sGC, contributes to the development and progression of this chronic hypertension and is likely a responsible mechanism for the hypertension-induced end-organ damage in this model (McIntyre et al., 1997, 1999; Ma et al., 2001; Ju et al., 2003; Stasch et al., 2006). The gene discussed is SGCB; the disease is hypertensive disorder.