Clinical hypertensive vascular disease is the result of complex alterations in the biology of the cellular components of the arterial wall. In this review, the hypothesis will be put forth that elevated blood pressure induces an inflammatory state in the arterial wall through both humoral and mechanical signaling pathways. The generation of reactive oxygen species and subsequent upregulation of redox-sensitive proinflammatory gene products are common endpoints of these pathways. Subsequent adaptive and maladaptive responses of the wall occur as a result of the integration of the humoral and mechanical stimuli.
Vascular complications of diabetes represent the leading cause of morbidity and mortality in affected patients. Production of reactive oxygen species is increased in diabetic patients, especially in those with poor glycemic control. Reactive oxygen species affect vascular smooth muscle cell growth and migration, endothelial function, including abnormal endothelium-dependent relaxation and expression of a proinflammatory phenotype, and modification of the extracellular matrix. All of these events contribute to the development of diabetic microvascular and macrovascular complications, suggesting that the sources of reactive oxygen species and the signaling pathways that they modify may represent important therapeutic targets.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.