Vasodilator Response to Systemic But Not to Local Hyperinsulinemia in the Human Forearm

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Insulin-mediated vasodilation has been proposed as an important determinant of whole-body insulin-stimulated glucose disposal. However, it is not clear whether the vasodilator effect of insulin results from a direct action of the hormone or whether alternative mechanisms are involved. To better characterize the mechanism of insulin-mediated vasorelaxation, we compared forearm blood flow (FBF) responses to local (intra-arterial) and systemic (intravenous, euglycemic clamp) hyperinsulinemia in 10 healthy lean subjects using venous occlusion plethysmography. In addition, we assessed the effect of nitric oxide (NO) synthase inhibition by NG-monomethyl-L-arginine (L-NMMA) on the vasodilator and metabolic responses to hyperinsulinemia. Similar forearm concentrations of insulin were achieved during local and systemic infusion (231 +/- 39 versus 265 +/- 22 [micro sign]U/mL; P=0.54). Of note, FBF did not change significantly in response to local hyperinsulinemia (from 2.6 +/- 0.3 to 2.4 +/- 0.3 mL [middle dot] min-1 [middle dot] dL-1; P=0.50). In contrast, systemic hyperinsulinemia caused a 52% increase in FBF (from 2.5 +/- 0.2 to 3.8 +/- 0.5 mL [middle dot] min-1 [middle dot] dL-1; P<0.004), which was reversed by L-NMMA (FBF decreased from 3.8 +/- 0.5 to 2.3 +/- 0.2 mL [middle dot] min-1 [middle dot] dL-1; P=0.004). We conclude that systemic, but not local, hyperinsulinemia induces vasodilation in the forearm. Our findings suggest that insulin-mediated vasodilation is not due solely to a direct stimulatory effect of insulin but involves additional mechanisms activated only during systemic hyperinsulinemia. (Hypertension. 1998;32:740-745.)

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