Fig. 3

Postpartum effects of AT1-AA blockade in preeclampsia on cardiac mitochondrial complexes and function. Mitochondria were isolated from hearts 10-week postpartum of rats that underwent normal pregnancy (NP), RUPP-induced preeclampsia, or the RUPP procedure and treatment with ‘n7AAc’ to inhibit AT1 autoantibodies (AT1-AA). A representative Western blot for respiratory complexes showing a reduction in levels of complex IV with RUPP-induced preeclampsia and recovery with AT1-AA blockade. B complex IV activity is reduced postpartum in mitochondria from RUPP rats compared to NP or RUPP + ‘n7AAc’. *p ≤ 0.05 was considered statistically significant (n = 6–9). C states 2, 3, and 4 respiration showing an overall reduction in mitochondria of RUPP rats postpartum compared to NP or RUPP + ‘n7AAc’. *p ≤ 0.05 was considered statistically significant (n = 3) D mitochondrial membrane potential with state 2 respiration measured by safranin uptake. *p ≤ 0.05 was considered statistically significant (n = 3–5). Note that statistical comparisons between normal pregnant (NP) postpartum, RUPP postpartum, and RUPP + AT1-AA inhibition (‘n7AAc’) postpartum was analyzed by a one-way ANOVA with Bonferoni’s post hoc test for figures B–D