The model shown in Figure 2 was tested using pressor levels of angiotensin II with renovascular responses (or in some experiments contractile responses to isolated preglomerular vascular smooth muscle cells) as the outcome measure and, therefore, applies to sympathetic regulation of renal vascular smooth muscle cells; however, we hypothesize that similar coincident signaling involving α2-ARs may occur in renal epithelial cells and may contribute directly to sodium retention and hypertension independent of renovascular changes (Figure 2). The gene discussed is AGT; the disease is Hypertension.