The vascular endothelium is a monolayer of cells between the vessel lumen and the vascular smooth muscle cells. Nitric oxide (NO) is a soluble gas continuously synthesized from the amino acid L-arginine in endothelial cells by the constitutive calcium-calmodulin-dependent enzyme nitric oxide synthase (NOS). This substance has a wide range of biological properties that maintain vascular homeostasis, including modulation of vascular dilator tone, regulation of local cell growth, and protection of the vessel from injurious consequences of platelets and cells circulating in blood, playing in this way a crucial role in the normal endothelial function. A growing list of conditions, including those commonly associated as risk factors for atherosclerosis such as hypertension, hypercholesterolemia, smoking, diabetes mellitus and heart failure are associated with diminished release of nitric oxide into the arterial wall either because of impaired synthesis or excessive oxidative degradation. The decreased production of NO in these pathological states causes serious problems in endothelial equilibrium and that is the reason why numerous therapies have been investigated to assess the possibility of reversing endothelial dysfunction by enhancing the release of nitric oxide from the endothelium. In the present review we will discuss the important role of nitric oxide in physiological endothelium and we will pinpoint the significance of this molecule in pathological states altering the endothelial function.

It is well known that cardiovascular disease is the leading cause of mortality in the western societies. A number of risk factors such as family history, diabetes, hypertension, obesity, diabetes, smoking and physical inactivity are responsible for a significant proportion of the overall cardiovascular risk. Interestingly, recent data suggest there is a gradient in the incidence, morbidity and mortality of cardiovascular disease across the spectrum of socioeconomic status, as this is defined by educational level, occupation or income. Additionally, dietary mediators seem to play significant role in the pathogenesis of cardiovascular disease, mediating some of the discrepancies in atherosclerosis among different socioeconomic layers. Therefore, in the present article, we aim to review the association between socioeconomic status and cardiovascular disease risk factors and the role of different dietary mediators.

White-coat hypertension (WCH) is a frequent condition particularly in children and elderly individuals. The prognostic significance of WCH is still a matter of debate. The present study was designed to systematically review cohort studies and assess the effects of WCH compared with normotension and sustained HTN on cardiovascular events and death, stroke, and all-cause mortality. We systematically searched the electronic databases, MEDLINE, PUBMED, EMBASE, and Cochrane for prospective cohort studies, which evaluated participants with office, and ambulatory, and/or home blood pressure. We included 14 studies with a total number of 29 100 participants (13 538 normotensive patients, 4806 with WCH and 10 756 with sustained HTN) with mean age of 59 years and follow-up of 8 years. Individuals with WCH had higher rates of cardiovascular disease morbidity and mortality but not significantly different all-cause mortality and stroke risk compared with normotensive patients. Cardiovascular disease morbidity and mortality, all-cause mortality, and stroke rates were significantly increased in patients with sustained HTN compared with WCH. The cardiovascular morbidity and mortality associated with WCH may be slightly higher compared with normotension but well below the risks associated with sustained HTN.