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. 2019 Jul 5;26:101271. doi: 10.1016/j.redox.2019.101271

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© 2019 The Authors. Published by Elsevier B.V.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 6 — Sulforaphane improves both endothelium-derived hyperpolarizing factor (EDHF)- and NO-mediated components of endothelial vasodilation in arteries from aged rats and human patients. Effects of sulforaphane (SFN, 10 μM) or the vehicle (0.1% DMSO) on relaxation induced by acetylcholine (ACh) in mesenteric arteries (RMA) (A, D) and coronary arteries (RCA) (B, E) from aged (20 M) rats and in human penile resistance arteries (HPRA) (C, F) from patients with erectile dysfunction (ED). Upper panels show ACh-induced relaxations in the presence of N^G-nitro l-arginine methyl ester (l-NAME, 100 μM) and indomethacin (INDO, 10 μM) to isolate the EDHF component of endothelial vasodilation. Lower panels show ACh-induced relaxations in arteries contracted with KCl (25–50 mM) in the presence of INDO to isolate the NO component of endothelial vasodilation. Data are expressed as mean ± SEM of the percentage of maximal relaxation induced by papaverine (0.1 mM). n indicates the number of animals (A, B, D, E) or patients (C, F). ***p < 0.001 vs. l-NAME + INDO or vs K⁺+ INDO by two-factors ANOVA test.