It is exacerbated when the pro-inflammatory arm of the renin-angiotensin system (RAS), the Angiotensin II/AT1R axis is activated either to maintain efferent arteriolar tone and hence GFR (Figure 4) as occurs in hypertension (Simons et al., 1994; Keller et al., 2003) or by activation of the renal G-coupled protein receptor, GRP91, by high glucose levels as occurs in diabetes mellitus (Peti-Peterdi, 2010). This evidence concerns the gene AGTR1 and hypertensive disorder.