PPARs in the Renal Regulation of Systemic Blood Pressure

Figure 1

Schematic representation of the RAAS cascade. The main signals activating the RAAS are the reduced nephron perfusion due to lowered arterial mean pressure and the hypovolemia-induced decrease in intratubular sodium/chloride load. Kidney JGA cells produce renin, which activates the RAAS cascade, yielding two main effector molecules, angiotensin II (AngII) and aldosterone. Other vasoactive angiotensins can also be produced from Ang-II by the action of different aminopeptidases (APs). The main ouputs of RAAS activation are arteriolar vasoconstriction and fluid retention, which both elevate mean arterial blood pressure. PPAR$\gamma$ is expressed in JGA, the source of renin and in the distal collecting ducts, targets of aldosterone. Histological image shows a renal glomerule with the longitudnal section of the afferent arteriole in mouse kidney (hematoxylin-eosin staining, N: 400x).