It is very likely that VSMC ENaC protein expression and/or function may be altered in hypertension because many of the “usual suspects” implicated in hypertension (i.e., endothelin, aldosterone, angiotensin II, inflammatory cytokines, reactive oxygen species, and nitric oxide, dietary salt) regulate tubular ENaC and neuronal ASIC channel expression (Gilmore et al., 2001; Mamet et al., 2002, 2003; Beutler et al., 2003; Amasheh et al., 2004; Barmeyer et al., 2004; Drummond et al., 2006; Helms et al., 2008; Jernigan et al., 2008, 2009; Pavlov et al., 2010; Chung et al., 2011). This evidence concerns the gene AGT and hypertensive disorder.