Background: Obesity is a major cardiovascular risk factor which dramatically impairs
endothelium-dependent vasodilation and leads to hypertension and vascular damage. The
impairment of the vasomotor response to extracellular autacoids, e.g. acetylcholine, mainly
depends on the reduced nitric oxide (NO) bioavailability, which hampers vasorelaxation in large
conduit arteries. In addition, obesity may affect endothelium-dependent hyperpolarization
(EDH), which drives vasorelaxation in small resistance arteries and arterioles. Of note,
endothelial Ca 2+ signals drive NO release and trigger EDH.
Methods: A structured search of bibliographic databases was carried out to retrieve the
most influential, recent articles on the impairment of vasorelaxation in animal models of obesity,
including obese Zucker rats, and on the remodeling of the endothelial Ca 2+ toolkit under
conditions that mimic obesity. Furthermore, we searched for articles discussing how dietary
manipulation could be exploited to rescue Ca 2+ -dependent vasodilation.
Results: We found evidence that the endothelial Ca 2+ could be severely affected by
obese vessels. This rearrangement could contribute to endothelial damage and is likely to be
involved in the disruption of vasorelaxant mechanisms. However, several Ca 2+ -permeable
channels, including Vanilloid Transient Receptor Potential (TRPV) 1, 3 and 4 could be
stimulated by several food components to stimulate vasorelaxation in obese individuals.
Conclusion: The endothelial Ca 2+ toolkit could be targeted to reduce vascular damage and
rescue endothelium-dependent vasodilation in obese vessels. This hypothesis remains,
however, to be probed on truly obese endothelial cells.