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. 2018 Feb 16;7(4):e007675. doi: 10.1161/JAHA.117.007675

Figure 5.

Figure 5

Contribution of nitric oxide synthase (NOS) and endothelium‐derived hyperpolarization (EDH) in resistance vessel endothelial function of female mice. Endothelium‐dependent acetylcholine‐induced relaxation was evaluated after NOS inhibition with L‐NAME (LN) alone, with the endothelial K+ channels blockers apamin (Apa) and TRAM34 (Tram) to inhibit EDH or with vehicle (Veh) in small mesenteric arteries of control, obese, and hyperlipidemic female EC‐MR–intact mice (EC‐MR +/+; A through C) or knockout mice (EC‐MR −/−; D through F). G, Area under the curve (AUC) represents the relative contribution of NOS and EDH in females and shows that females depend more on EDH and that the reduction in EDH in obesity and hyperlipidemia is compensated for with an increased NOS component when EC‐MR is deleted. Two‐factor ANOVA, *P<0.05 vs EDH in control EC‐MR +/+; # P<0.05 vs nitric oxide in EC‐MR +/+ under the same risk factor condition. EC‐MR indicates mineralocorticoid receptors in endothelial cells.