Endothelial dysfunction as a consequence of a variety of common cardiovascular disease risk factors is thought to be associated with increased reactive oxygen species (ROS) and the subsequent decrease in vascular bioavailability of nitric oxide (NO). In this article we give a detailed discussion of evidence of the impact of oxidative-nitrosative stress during maternal pregnancy on fetal development in animal models and also the association with the onset of cardiovascular conditions in adult humans. We highlighted specifically the presence of ROS in circulating blood as the key intermediary related to vascular injury and organ dysfunction, the evidence that red blood cells regulate the arteriolar microcirculation, coupling oxygen delivery with blood flow, and highlighting their role in NO bioavailability. The unique nature of relationship between cell-signalling, transcriptional mechanisms and oxidative-nitrosative stress in the progression of coronary heart disease has also been discussed in greater detail. We have also discussed the emerging concepts that pharmacological prevention of cardiovascular events in the future might consists of the control of classical risk factors with specific interventions targeting oxidative stress while simultaneously improving NO production.
Cardiac development; Developmental programming; Oxidative stress