Insulin action is associated with endothelial function in hypertension andtype 2 diabetes

A primary defect in the vascular action of insulin may be a key intermediat e mechanism that links endothelial dysfunction with reduced insulin-mediate d cellular glucose uptake in metabolic and cardiovascular disorders. The pr esent study was designed to characterize more fully the relations between i nsulin action and endothelial function in male patients with essential hype rtension (H, n=9) or type 2 diabetes (D, n=9) along with healthy control su bjects (C) matched for age, body mass index, and lipid profile. They attend ed for measurement of whole-body insulin sensitivity (MCR) by the hyperinsu linemic clamp technique (day 1) and forearm vasoreactivity in response to i ntra-arterial infusions of insulin/glucose (day 2) and N-G-monomethyl-L-arg inine (L-NMMA) and norepinephrine (day 3) by bilateral venous-occlusion ple thysmography. Results expressed as mean+/-SE MCR (mL/kg per minute) were 7. 22+/-0.99 (C), 6.32+/-0.78 (H), and 5.06+/-0.53 (D). Insulin/glucose-mediat ed vasodilation (IGMV) was 17.1+/-5.6% (C), 17.2+/-5.5% (H), and 12.3+/-6.4 % (D). L-NMMA vasoconstriction (LNV) was 37.9+/-5.1% (C), 37.5+/-2.3% (H), and 33.6+/-2.8% (D). There were no significant differences among groups for these parameters. Pooled correlation analyses revealed associations betwee n MCR and IGMV (r=0.46, P<0.05), MCF, and LNV (r=0.44, P<0.05), and IGMV an d LNV (r=0.52, P<0.01). This study supports functional coupling between ins ulin action (both metabolic and vascular) and basal endothelial nitric oxid e production in humans.