It is tempting to speculate that increased vasoconstriction and loss of endotheliumdependent
vasodilation might be etiological factors of elevated blood pressure in the insulinresistant …

We have reported that a deficiency of tetrahydrobiopterin (BH4), an active cofactor of
endothelial NO synthase (eNOS), contributes to the endothelial dysfunction through reduced …

To investigate underlying mechanisms responsible for the impaired nitric oxide (NO)-
dependent vascular relaxation in the insulin-resistant state, we examined production of both …

Although insulin-resistant states have been associated with endothelial dysfunction due to
increased vascular oxidative stress, the underlying mechanisms are pooly understood …

Insulin stimulates production of NO in vascular endothelium via activation of
phosphatidylinositol (PI) 3-kinase, Akt, and endothelial NO synthase. We hypothesized that …

Dysfunction of the endothelium in large-and medium-sized arteries plays a central role in
atherogenesis. The insulin resistance syndrome encompasses more than a subnormal …

OBJECTIVE—Insulin resistance is an independent risk factor for the development of
cardiovascular atherosclerosis. A key step in the development of atherosclerosis is …

Insulin activation of the phosphatidylinositol 3-kinase (PI3K) pathway stimulates glucose
uptake in peripheral tissues and synthesis of nitric oxide (NO) in the endothelium. Insulin …

Impairment of nitric oxide-dependent vascular relaxation is a characteristic feature of the
insulin-resistant state. To understand those mechanisms, we examined imbalance of …

Deficiency of tetrahydrobiopterin (BH4) in the vascular tissue contributes to endothelial
dysfunction through reduced eNOS activity and increased superoxide anion (O2−) …