Reactive oxygen species (ROS) are a class of molecules that includes O2
•- (superoxide anion), ONOO– (peroxynitrite), •OH
(hydroxyl radical), and H2O2 (hydrogen peroxide). Members of ROS play an important role in the pathogenesis of vascular
disease in that they contribute to the development of vascular complications including endothelial dysfunction, inflammation,
remodeling, apoptosis, endothelial cell migration, and activation of adhesion molecules. These events are significant to the
pathogeneses of distinctive cardiovascular diseases such as hypertension, atherosclerosis and diabetes mellitus. Many
enzymatic systems on the vascular wall may contribute to ROS generation, including nicotinamide adenine dinucleotide
phosphate (NADPH) oxidase, mitochondrial enzymes and uncoupled endothelial nitric oxide (NO) synthase (eNOS). Among
ROS generated in vascular cells, O2
•- and H2O2 are especially important for their association to elevations in intracellular
calcium levels, reduction in NO bioavailability, lipoperoxidation, and activation of redox-signaling pathways, which all lead to
vascular remodeling and contraction. In addition to smooth muscle and endothelial cells, the perivascular adipose tissue
(PVAT) is also recognized as a rich source of ROS, contributing to vascular dysfunction in many pathologies.
The current special issue of Current Hypertension Reviews is composed of articles that discuss the strong relationship
between oxidative stress and vascular disease with a focus on the biology of ROS signaling in vascular cells and how oxidative
stress contributes to vascular damage in several circumstances. In this special issue, the first article discusses basic aspects of
vascular oxidative stress. The molecular mechanisms that lead to vascular dysfunction and the role of the renin-angiotensin
system (RAS) in this process are discussed by Do Vale and Tirapelli [1]. A brief update on the vascular sources of ROS, crucial
to multiple aspects of vascular damage during hypertension, is provided by Pinheiro and Oliveira-Paula [2]. The review by
Phillips et al. concentrates on detailing mechanisms of vascular function, the role of oxidative stress in vascular biology and
how ethanol consumption may alter endothelial and smooth muscle cell function as well as microvascular function [3].
Most of the systemic blood vessels are surrounded by the perivascular adipose tissue (PVAT). Healthy PVAT is anticontractile
and anti-inflammatory, but a dysfunctional PVAT has been suggested to link cardiometabolic risk factors to vascular
dysfunction. In this context, the final paper in the special issue by Victorio and Davel discusses new findings describing major
sources of ROS in PVAT including mitochondria, NADPH oxidase and eNOS uncoupled, and finally, changes in ROS
production affecting vascular function in the presence of cardiometabolic risk factors and diseases [4]. The role of ROS and
RAS in vascular toxicity induced by metals is discussed by Vassallo et al. in a review addressing the impact of mercury, lead
and cadmium in the vascular endothelium with a new perspective, calling into the question the impact of low doses of these
metals on the vascular function [5].
We thank the authors for all the considerable time, efforts and expertise they committed to the preparation of their
manuscripts. The papers presented in this issue provide considerable insight into the role of ROS in the pathogenesis of
vascular disease, which we hope, the readers will find both informative and stimulating.