The responses of the iliac artery to insulin: direct delayed nitric oxide-mediated dilatation

Abstract

T he aim of the study was to determine the effect of insulin on a conduit artery. In a closed-off test segment of iliac artery in vivo in anaethetised pigs, pressure was kept constant. During the first 10 minutes of exposure to hyperinsulinaemic blood, the test segment diameter was 3.63±0.64 mm (mean ± SD). Dilatation occurred after 10 minutes when the test segment diameter increased to 3.80±0.62 mm (mean ± SD), p=0.0006, n=10. The increase in diameter with the vehicle for insulin in blood was -0.0775±0.116 mm (mean ± SD, n=6) and with hyperinsulin in blood was 0.165±0.124 mm (mean ± SD, n=10), p=0.0024. Dilatation with hyperinsulin was 0.229±0.116 mm (mean ± SD) versus insulin plus 250 µg/ml of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester hydrochloride (L-NAME), 0.041±0.026 mm (mean ± SD), p=0.0313, n=6. No evidence of arterial constriction was observed in the presence of L-NAME. We conclude that insulin has a direct relaxing effect on the smooth muscle in the wall of conduit artery, mediated by nitric oxide. Br J Diabetes Vasc Dis 2011;11:130-136.

Why Should be the Strategy of Type 2 Diabetes Treatment Radically Changed

“…In fatty tissue metformin impedes lipolysis and decreases elevated plasma-free fatty acids, restraining thus the lipotoxic injury associated with worsening of insulin resistance in various tissues including liver, vessels, skeletal muscles and beta pancreatic cells. In endothelial cells metformin decreases insulin resistance reflected by enhanced NO synthesis and vasodilation in peripheral tissues [24][25][26]. Thus, it seems that metformin's cardioprotective properties are explained by mechanisms independent on glycemic control, mainly by improvement of the insulin resistance and endothelial dysfunction.…”