Preserved endothelial-dependent and endothelial-independent skin vasodilator responses in relatives of type 1 diabetes patients.

Since increased plasma and cell levels of oxidative products have been found in non diabetic relatives of type 1 diabetic patients, we hypothesized the occurrence of an endothelial dysfunction in these subjects. To verify this hypothesis we investigated the skin blood flow responses to iontophoresis of both the endothelial-dependent vasodilator acetylcholine (ACh) and the endothelial-independent vasodilator sodium nitroprusside (SNP) in 31 non diabetic healthy relatives (DR) (14 siblings, 17 parents) of 17 type 1 diabetic patients. Twenty healthy control subjects (CS) without a family history of diabetes, matched for age (+/-5 years) and gender, were also investigated. DR and CS did not significantly differ either in basal skin blood flux (6.75+/-0.72 PU and 5.78+/-0.37 PU, respectively) or in skin vasodilator response to both ACh (728+/-53% and 711+/-44%, respectively) and SNP iontophoresis (758+/-71% and 731+/-64%, respectively). This finding is consistent with a preserved skin microvascular endothelial function in the studied subjects. However, since previous data suggest that both nitric oxide (NO) and prostacyclin released form the cutaneous vascular endothelium have an interchanging compensatory role in controlling the skin vasodilator response to ACh iontophoresis, our finding does not allow a defect in NO dependent skin vasodilatation to be excluded in the studied relatives of diabetic patients.