Skip to main content
. 2021 Mar 20;8(3):1933–1943. doi: 10.1002/ehf2.13219

Figure 1.

Figure 1

Finerenone treatment improved ovariectomy‐induced left ventricular (LV) diastolic dysfunction and improved oxidative stress‐related impairment of endothelium‐dependent relaxation of coronary arteries. (A–D) LV invasive haemodynamics in control mice (CTL, black circles, n = 4) and in mice after 4 months of ovariectomy (OVX, red squares, n = 7) without or with 1 month finerenone treatment (OVX + Fine, green triangles, n = 6). (A) LV end‐systolic pressure (LVESP). (B) LV end‐diastolic pressure (LVEDP), that is, LV filling pressure. (C) LV end‐systolic pressure–volume relation (LVESPVR), that is, LV contractility. (D) LV end‐diastolic pressure–volume relation (LVEDPVR), that is, LV compliance. (E–H) Relaxation of isolated coronary arteries from control mice (CTL, black circles, n = 5) and from mice after 4 months of ovariectomy (OVX, red squares, n = 6) without or with 1 month finerenone treatment (OVX + Fine, green triangles, n = 5). Relaxation induced (E) by acetylcholine (Ach), (F) by Ach in the presence of the NO synthase inhibitor l‐NG‐nitro‐arginine (L‐NNA) 10−4 mol/L, (G) by the NO donor sodium nitroprusside (SNP), and (H) by Ach after addition of apocynin 10−4 mol/L. Data are mean ± standard error of the mean. Statistics: one‐way ANOVA plus Tukey, **P < 0.01 and ***P < 0.001 vs. CTL; † P < 0.05 and †† P < 0.01 vs. OVX.