Metabolic syndrome (MetS) is associated with clustering of cardiovascular risk factors in individuals that may greatly increase their risk of developing coronary artery disease. Obesity and related metabolic dysfunction are the driving force in the prevalence of MetS. It is believed that obesity has detrimental effects on cardiovascular function, but its overall impact on the vasomotor regulation of small coronary arteries is still debated. We aimed to examine the impact of obesity on the vasomotor function of large conduit vessels and small coronary arterioles. We have found that in the brachial artery there was a positive correlation between flow-mediated (FMD)- and nitroglycerin (NTG)-induced dilations and body mass index (BMI) in obese patients. In animal model of diet-induced obesity, we demonstrated that due to the activation of soluble guanylate cyclase the sensitivity of vascular smooth muscle cells to nitric oxide is enhanced, which contributes to the enhanced coronary arteriolar dilations to nitric oxide donors. Our data indicate that in obesity arteries adapt to hemodynamic changes via upregulating cellular mechanism(s) intrinsic to the vascular wall. A better understanding of mechanisms that may contribute vascular adaptation may provide insight into the sequence of pathological events in obesity and may allow the harnessing of these effects for therapeutic purposes
