DOI: 10.3390/ijms20092155
Huige Li,1 Ning Xia,1 Solveig Hasselwander,1 and Andreas Daiber2
1Department of Pharmacology, Johannes Gutenberg University Medical Center, 55131 Mainz, Germany 2Center for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, Johannes Gutenberg University Medical Center, 55131 Mainz, Germany
Abstract
Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling. At the same time, resveratrol inhibits the synthesis of endothelin-1 and reduces oxidative stress in both endothelial cells and smooth muscle cells. Pathological stimuli-induced smooth muscle cell proliferation, vascular remodeling, and arterial stiffness can be ameliorated by resveratrol as well. In addition, resveratrol also modulates immune cell function, inhibition of immune cell infiltration into the vascular wall, and improves the function of perivascular adipose tissue. All these mechanisms contribute to the protective effects of resveratrol on vascular function and blood pressure in vivo. Sirtuin 1, AMP-activated protein kinase, and estrogen receptors represent the major molecules mediating the vascular effects of resveratrol.
Keywords: resveratrol, endothelium, endothelial nitic oxide synthase, sirtuin 1, cardiovascular disease, vascular function