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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Hypertension. 2019 Apr;73(4):849–858. doi: 10.1161/HYPERTENSIONAHA.118.12198

Figure 1: WD induces aortic, kidney artery, and microvessel endothelial stiffening as well as impairs endothelial relaxation dependent on the ECMR.

Figure 1:

A. Plasma aldosterone levels and kidney expression of MR. Aldosterone: N=6 for CD ECMR+/+, 7 for WD ECMR+/+ and 6 for WD ECMR−/−. Expression of MR: N=4 for CD ECMR+/+, 7 for WD ECMR+/+.and 6 for WD ECMR−/−. B. Pulse wave velocity and renal endothelial stiffness evaluated by atomic force microscopy using kidney vessel explants. Pulse wave velocity: N=6 for CD ECMR+/+, 8 for WD ECMR+/+and 11 for WD ECMR−/−. Endothelial stiffness: N= 3 for CD ECMR+/+, 3 for WD ECMR+/+ and 4 for WD ECMR−/−. C. Microvessel mechanical and functional studies. Microvessel stiffness evaluated with incremental moduli of elasticity using pressure myography in mesenteric vessels. Relaxation studies included vasorelaxation response to the endothelium-dependent dilator acetylcholine (ACh), vasorelaxation response to the endothelium-dependent dilator insulin (Ins) and vasorelaxation response to the vascular smooth muscle-dependent dilator sodium nitroprusside (SNP). N=6 for CD ECMR+/+, 7 for WD ECMR+/+ and 7 for WD ECMR−/−. Control diet (CD), Western Diet (WD). Data are expressed as means ± SEM. † P<0.05 vs CD; ‡ p<0.05 vs WD ECMR+/+.