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.
Hypertension causes a number of alterations of the coronary circulation which may influence the outcome of anaesthesia and surgery. These include changes in the architecture of the coronary vasculature, and impairments in coronary reserve and autoregulatory ability of the coronary microvasculature during decreases in perfusion pressure. Chronic hypertension may also alter endothelial regulation of vascular control. Many of the vasodilators used to treat hypertension may have unique effects on the coronary circulation which may become modified by chronic hypertension and cardiac hypertrophy. In this review, each of these areas are considered together with some unique aspects of endothelial/vascular smooth muscle interactions as they relate to acute and chronic hypertension, and to the pharmacological agents used in the treatment of hypertension.
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.