The Role of Obesity-Induced Perivascular Adipose Tissue (PVAT) Dysfunction in Vascular Homeostasis

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  Figure 1. Vasodilatory and hyperpolarizing effect of perivascular adipose tissue–derived factors (PVAT-derived factors) on vascular smooth muscle cells (VSMCs) and hyperpolarizing effect of PVAT-derived factors on endothelial cells. Adiponectin causes vasodilation by affecting adiponectin receptors (AR) in endothelial cells, which contributes to the activation of locations 5′ adenosine monophosphate-activated protein kinase (AMPK), which is responsible for the activation of endothelial NO synthase (eNOS). Enhanced NO concentration induces activation of cyclic guanosine monophosphate (cGMP), which is responsible for opening large-conductance calcium-activated potassium channels (BKCa). eNOS is present in both endothelial cells and adipocytes. Leptin activates leptin receptors (LR), which are responsible for activation of not only AMPK, but also endothelium-derived hyperpolarizing factor (EDHF), which activates BKCa. Moreover, AMPK independently activates BKCa and induces a hyperpolarization effect. Hydrogen sulfide (H2S) induces activation of BKCa in VSMCs and endothelial cells. Moreover, it induces a decrease in intracellular pH by the activation of Cl−/HCO3− ionic exchanger. Angiotensin…

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  Figure 2. The influence of obesity on PVAT-derived factors’ synthesis resulting in vascular dysfunction. (PVAT: perivascular adipose tissue, RAAS: renin–angiotensin–aldosterone system, NO: nitric oxide, H2S: hydrogen sulfide, H2O2: hydrogen peroxide, TNF–α: tumor necrosis factor α, and NA: noradrenaline).