Nongenomic action of aldosterone on colocalization of angiotensin II type 1 and type 2 receptors in rat kidney

Abstract

Previous in vitro studies have demonstrated that angiotensin II type 1 and type 2 receptors (AT1R and AT2R) are co-localized and can form AT1R/AT2R dimerization in rat proximal tubular cells. Aldosterone non-genomically enhances angiotensin II receptor dimerization. We found no other in vivo studies in the literature regarding the effect of aldosterone on colocalization of AT1R and AT2R in whole kidney. Male Wistar rats were intraperitoneally injected with either normal saline solution (sham group) or aldosterone (experimental group). Colocalization of renal AT1R and AT2R proteins was examined by double immunohistochemical staining. The colocalization of AT1R and AT2R proteins was more prominent in the glomerulus, distal convoluted tubules, and cortical collecting ducts while colocalization was weak and diffused in the proximal convoluted tubules and peritubular capillaries in both groups. Our in vivo study showed aldosterone did not alter a constitutive colocalization of AT1R and AT2R proteins in the renal cortex and medulla. However, these proteins were colocalized more prominently in the renal cortex.