1996
DOI: 10.1016/0735-1097(95)00522-6 View full text |Buy / Rent full text
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Abstract: Nitric oxide-mediated vasodilation is impaired in non-insulin-dependent diabetes mellitus. Vasoconstrictor prostanoids do not contribute significantly to vascular dysfunction. The attenuated response to exogenous as well as endogenous nitric oxide donors suggests that the abnormality is due to increased inactivation of nitric oxide or to decreased reactivity of the vascular smooth muscle to nitric oxide.

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“…This is in agreement with a study comparing subjects with type 2 diabetes (NIDDM) with normoglycaemic controls, in which both EDV and EIDV were found to be impaired in the diabetics [35]. Elevated glucose levels could impair EDV by several mechanisms, such as an activation of the polyol pathway resulting in a decline in the NO synthesis cofactor NADPH and a decline in the activity of the Na,KATPase, oxygen free radical formation and activa-tion of protein kinase C [36±39].…”
Section: Discussionsupporting
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“…This is in agreement with a study comparing subjects with type 2 diabetes (NIDDM) with normoglycaemic controls, in which both EDV and EIDV were found to be impaired in the diabetics [35]. Elevated glucose levels could impair EDV by several mechanisms, such as an activation of the polyol pathway resulting in a decline in the NO synthesis cofactor NADPH and a decline in the activity of the Na,KATPase, oxygen free radical formation and activa-tion of protein kinase C [36±39].…”
Section: Discussionsupporting
“…First, peripheral blood flow was not measured in the study subjects. As vasodilation is impaired in patients with insulin resistance and diabetes, 27 the impaired aerobic capacity that we observed might be due to the decreased blood flow to skeletal muscle. However, Hallsten et al 28 demonstrated that the peripheral blood flow to skeletal muscle in obese and insulin-resistant subjects was not lower than that in controls, even during exercise.…”
Section: Control Metsmentioning
“…McVeigh et al 37 reported decreased responses to acetylcholine and GTN in the forearm vascular bed. 37 These findings have been confirmed in a more recent study, 38 and suggest either impaired vascular smooth muscle sensitivity to NO or its increased inactivation. However, they support the concept of reduced functional activity of the vascular NO system in patients with type 2 diabetes mellitus.…”
Section: Type 2 Diabetes Mellitus and Endothelial Dysfunctionmentioning