Hemodynamic alterations in diabetes are believed to arise as a result of hyperglycemia-induced metabolic abnormalities and elaboration of vasoactive factors including ETs. There is great heterogeneity in findings from microcirculation studies in humans. Study of nailfold microcirculation has revealed elevated as well as reduced blood velocity in diabetic patients when compared to healthy subjects. Reduced blood velocity has also been observed in gastric mucosal blood flow studies. Much of the inconsistency in such studies can be attributed to duration of diabetes, interstudy variability, and limitations of techniques used for measurement of blood flow.
In parallel to in vivo blood flow studies, ex vivo measurement of blood vessel responsiveness to ETs has produced conflicting results. Depending on the relative distribution of ETA and ETB receptors in the vascular bed, responsiveness has been shown to be attenuated as well as exaggerated. Limited animal model studies suggest that diabetes leads to alteration of ET responsiveness. Based on existing evidence, however, diabetes is believed to cause vasoconstriction and reduced blood flow early in target organs of chronic complications. These hemodynamic alterations are mediated by increased vasoconstrictors such as ETs and reduced vasodilators including NO. Administration of ET-1 in humans has demonstrated reduced coronary and renal blood flow and increased vasoconstriction. Furthermore, we have demonstrated increased diabetes-induced vasoconstriction in the retina which was normalized with ET receptor antagonist .
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