Skip to main content
. Author manuscript; available in PMC: 2019 May 17.
Published in final edited form as: Curr Hypertens Rep. 2018 Aug 17;20(10):89. doi: 10.1007/s11906-018-0889-4

Figure 1: Mechanisms of mitoprotection by renin angiotensin aldosterone system blockade:

Figure 1:

Both angiotensin-I converting enzyme inhibitors (ACEi) and angiotensin-II AT1 receptor blockers (ARB) decrease angiotensin-II levels, thereby preventing its actions through AT2 receptors located in the inner mitochondrial membrane. Experimental studies have shown that treatment with ACEi and ARBs decreases mitochondrial reactive oxygen species (ROS) production and uncoupling protein (UCP)-2 content, and increases biogenesis, nitric oxide synthase (mtNOS), gluthatione (GSH), and superoxide dismutase (SOD) activity, mitophagy, and adenosine triphosphate (ATP) production.