Journal
JOURNAL OF VASCULAR RESEARCH
Volume 43, Issue 4, Pages 309-320Publisher
KARGER
DOI: 10.1159/000093196
Keywords
diabetes; endothelial dysfunction; insulin; microcirculation; nitric oxide; oxidative stress; tetrahydrobiopterin
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Diabetes-induced vascular dysfunction has mainly been studied in males. However, the mechanisms involved may not correspond to those in females. Here we analyzed the effects of tetrahydrobiopterin (BH4) and chronic insu in on the physiology of mesenteric arterioles of alloxar-diabetic female rats. The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy), nitric oxide synthase (NOS) activity (conversion of L-arginine to L-citrulline), eNOS gene expression (RT-PCR), NO production (diaminofluorescein), reactive oxygen species (ROS) generation (intravital fluorescence microscopy) and Cu/Zn superoxide dismutase (SOD) activity (spectrophotometry) and gene expression (RTPCR). The reduced endothelium-dependent vasodilation of diabetic females was corrected by both BH4 and insulin. NOS activity was decreased by diabetes, but insulin did not correct it. However, NOS expression was not modified by either diabetes or insulin. Arterioles of diabetic rats exhibited lower NO production, which was fully corrected by BH4 and only partially by insulin. ROS generation was increased in diabetic rats, and both BH4 and insulin normalized it. Diabetes did not change SOD activity and gene expression. However, insulin increased SOD activity but not its expression. Our data suggest that, similarly to males, endothelial dysfunction in female diabetic rats involves an altered ROS/NO imbalance. In contrast to males, however, insulin does not regulate NOS in the microcirculation of diabetic females. Copyright (c) 2006 S. Karger AG, Basel.
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