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. 2019 Nov 13;318(2):R256–R262. doi: 10.1152/ajpregu.00179.2019

Fig. 3.

Fig. 3.

Angiotensin II type 1 receptor agonistic autoantibody (AT1-AA) inhibition reduced mitochondrial oxidative stress (mtROS) production in reduced uterine perfusion pressure (RUPP) kidney. Respiration rates were measured in isolated mitochondria using the Oxygraph 2K, and mtROS (H2O2) was measured using Amplex red assay with a fluorescent microplate reader. State 3 respiration (A) and maximal respiration (B) in RUPPs treated with AT1-AA inhibitory peptide [′n7AAc′; n = 9 (A) and 6 (B)] vs. RUPPs [n = 6 (A) and 6 (B)]. Furthermore, AT1-AA inhibition significantly reduced mtROS production in RUPPs treated with ′n7AAc′ (n = 3) vs. RUPPs (n = 4) (C). Data are presented as means ± SE. *P < 0.05 vs. RUPP, Student’s t-test.