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. 2016 Aug 10;68(3):726–735. doi: 10.1161/HYPERTENSIONAHA.116.07911

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© 2016 The Authors.

Hypertension is published on behalf of the American Heart Association, Inc., by Wolters Kluwer. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDervis License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 3. — Reduced HSP90 expression and endothelial nitric oxide synthase (eNOS) uncoupling after β-AR overstimulation: prevention by mineralocorticoid receptor blockade. Diaminofluorescein (DAF-2) fluorescence (A), protein expression of total eNOS (B), dimer:monomer eNOS ratio (C), HSP90 (D), and hidroethidine (DHE) fluorescence (E) obtained in aorta from control (CT) and isoproterenol (ISO) groups without or with spironolactone (SPI) treatment. Protein expression was calculated as percentage of CT group. Representative images (20×, bar=100 µm) of DAF-2 and DHE fluorescence are shown in left side of A and E, respectively. In A, E=endothelium. The DHE fluorescence signal was evaluated under basal condition or after incubation with Nω-nitro-L-arginine methyl ester (L-NAME) (1 mmol/L) or MnTMPyP (25 µmol/L). Data represent mean±SEM; number of animals used for each group is indicated in the bars. Two-way ANOVA: P<0.05 *vs CT; +vs SPI; #vs ISO.