Skip to main content
. Author manuscript; available in PMC: 2021 Jul 1.
Published in final edited form as: Hypertension. 2020 Jun 1;76(1):121–132. doi: 10.1161/HYPERTENSIONAHA.119.13942

Figure 3.

Figure 3.

Adenovirus-mediated overexpression of proximal tubule-specific, mitochondria-targeting mito-ECFP/Ang II induces mitochondrial oxidative stress (OCR, oxygen consumption rate) and glycolysis stress (ECAR, extracellular acidification rate) responses in living mPCT cells in a real-time manner. A & D, the concentration-dependent increases in mitochondrial OCR responses to extracellular Ang II added to the medium, and the maximal OCR effect at 10 nM was blocked by losartan, but not by PD123319. B, showing that the expression of mito-ECFP/Ang II increased the OCR response, and the effect was blocked by losartan, but not PD123319. C, showing that the concurrent coexpression of mitochondria-targeting mito-AT2R/GFP significantly attenuated the effect of mito-ECFP/Ang II on OCR, and the effect of mito-AT2R/GFP on OCR was blocked by PD123319. E, showing that the effect of mito-ECFP/Ang II on OCR was attenuated by mito-TEMPO, a mitochondria-targeting superoxide scavenger. F, showing that the nonselective NOS inhibitor L-NAME alone moderately increased the OCR response. **P<0.01 vs. control or untreated cells. ++P<0.01 vs. mito-ECFP/Ang II. Results represent 10 samples (wells) of two separate experiments.