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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Curr Hypertens Rep. 2013 Feb;15(1):17–24. doi: 10.1007/s11906-012-0316-1

Figure 1. (A) Principal scheme of direct stimulatory effect of Ang II and aldosterone on ENaC in the distal nephron.

Figure 1

MR – mineralocorticoid receptors; AT1R – Angiotensin II type 1 receptors, PKC – protein kinase C; NOX – NADPH oxidase complex; ROS – reactive oxygen species; AA – arachidonic acid; EETs – Epoxyeicosatrienoic acids. ↑Po – increased ENaC open probability; ↑N – increased ENaC expression at the apical plasma membrane. This scheme is modified from Mamenko M, Zaika O, Ilatovskaya DV, et al. (2012) Angiotensin II Increases Activity of the Epithelial Na+ Channel (ENaC) in Distal Nephron Additively to Aldosterone. J Biol Chem 287: 660–671. © the American Society for Biochemistry and Molecular Biology. (B) Ang II actions on major transport proteins in the distal nephron. Physiological consequences of these actions are outlined on the right.