Overconsumption of sugar has recently been implicated in the pathogenesis of cardiovascular pathologies. Previously, we managed to confirm that an acute hyperglycemia may decrease vascular function even in healthy young adults and that oxidative stress seems to be the main factor leading to vascular dysfunction. According to recent literature on other tissues, this oxidative stress would be dependent of sodium-glucose cotransporters (SGLT/SMIT) activation by hyperglycemia.

Consequently, this study investigated the potential expression of these cotransporters in vascular tissues and their involvement in oxidative stress impairments of vascular function during acute hyperglycemia.

First SGLT1, SGLT2 and SMIT1 expressions were evaluated, in aortas of Wistar rats by Western blot. Then vascular function was evaluated in aortic rings from Wistar rats (n=20) mounted in an organ chamber to evaluate endothelium dependent vasodilatation (ACh 10⁻¹⁰ to 10⁻⁵M). This evaluation was performed in normoglycemic (11mM) and hyperglycemic (100mM) conditions in presence or not of an antioxidant (NAC 10μM) or an NADPH inhibitor (Apocynin 10μM). Implication of SGLT/SMITs and glucose transporter (GLUT) activities were assessed through their inhibition by respectively phlorizin (1mM) and phloretin (1mM).

Our first results managed to confirm the deleterious effects of hyperglycemia on vascular function and the role of oxidative stress was pointed out through the protective effects of antioxidants. Secondly, we managed to demonstrate that SGLT1/2 and SMIT1 are expressed in aortic tissues. Moreover, SGLT/SMIT inhibition by phlorizin managed to protect endothelial function in hyperglycemic condition. Such protective effect was not observed when GLUT transporters were inhibited.

Those results points out the involvement of sodium glucose cotransporters in the oxidative damaged induced by hyperglycemia while excluding GLUT implication.