Abstract
INTRODUCTION: Few reports have mentioned the effect of etomidate on the aortas of insulin-resistant (IR) rats. In this study, we investigated the effect of etomidate on isolated IR aortas of rats, and explored its underlying mechanism. MATERIAL AND METHODS: The IR rat model was established through feeding with a high-fructose diet. The systolic blood pressure (SBP) was measured by the tail-cuff method before grouping and at the end of the 8-week feeding; blood samples were also obtained for analysis. Thoracic aorta rings of IR rats were isolated and suspended in a tissue bath. The tensile force was recorded isometrically. The effect of etomidate on provoked contraction of the rings was assessed with or without a potassium channel blocker or NO synthase inhibitor. RESULTS: Etomidate-induced relaxation in IR rings was greater than normal control (NC) rings (all p < 0.001 with etomidate log M of -4 to -6). NG-nitro-L-arginine methyl ester (L-NAME, an NO synthase inhibitors) inhibited etomidate-induced relaxation in NC rings, but had no effect on the IR rings (all p < 0.001 with etomidate log M of -4 to -6). Pre-incubation with glibenclamide (Gli, a potassium channel blocker) significantly inhibited etomidate-induced relaxation in NC and IR rings (all p < 0.001 with etomidate log M of -4 to -6), and had no inhibited effect on endothelial denuded aortic rings. CONCLUSIONS: Insulin resistance increased etomidate-induced relaxation in rat aortas. Etomidate causes vasodilation in IR rat aortas via both endothelium-dependent and independent ways; impaired NO-mediated relaxation was disrupted and ATP-sensitive potassium (K(ATP)) channel-mediated relaxation may be involved in the endothelium-dependent relaxation of etomidate in IR rats.