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Highlights the crucial role of impaired endothelial nitric oxide generation and excess reactive oxygen species in the development of coronary microvascular dysfunction in diabetes.
The risk of cardiovascular disease is markedly elevated in individuals with diabetes, representing the primary cause of morbidity and mortality in these diabetic patients (1). More specifically, individuals with diabetes display dysfunctions in the regulation of blood flow in coronary arterioles (2,3). Importantly, impairments in the appropriate vasodilatory response of myocardial arterioles to various pharmaceutical and physical stimuli can be present even if there is no discernible atherosclerotic blockage in these blood vessels (4,5). Moreover, increased flow-mediated dilation (FMD) in coronary arterioles is an important regulatory mechanism for controlling arteriolar diameter and blood flow in response to changes in wall shear stress, and this mechanism is also impaired in conditions of glucose dysregulation (6,7). While the underlying etiology for the dysfunctions in the coronary microcirculation in diabetes is certainly multifactorial, the contribution of impairments in the endothelial nitric oxide (NO)–generating system and their association with the excess generation of reactive oxygen species (ROS) appears to be crucial in the development of these vascular abnormalities. For example, the impairment of the induction of vasodilation in coronary arterioles in the db/db mouse, a model of obesity-associated insulin resistance and type 2 diabetes, is related to limitations in NO availability (8,9). It is of great interest that NO availability can be compromised by interactions with superoxide anion, with a …
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Erik J. Henriksen (2014) studied this question.
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