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 Ca2+ 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 Ca2+ toolkit under conditions that mimic obesity.
Furthermore, we searched for articles discussing how dietary manipulation could be exploited to rescue
Ca2+-dependent vasodilation.
Results:
We found evidence that the endothelial Ca2+ 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 Ca2+-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 Ca2+ 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.
Regional Fat Pad Growth and Cellularity in Obese Zucker Rats: Modulation by Caloric Restriction
