Na+/H+ exchanger inhibitor prevented endothelial dysfunction induced by high glucose
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Updated: Aug 18, 2026

A Microfluidic System for Modeling Endothelial Dysfunction under Combined Physiological Pulsatile Shear Stress and Oscillatory Hyperglycemia
Published on: May 12, 2026
Wang Shuang-Xi1, Liu Li-Ying, Hu-Min
1Department of Pharmacology, Xiang-Ya Medical College, Central South University, Hunan, People's Republic of China.
Abstract:
The aims of this study were to examine whether cariporide, a selective Na+/H+ exchanger inhibitor, has protective effects against endothelial dysfunction induced by high glucose in vitro and to investigate the potential mechanisms. Exposure of rat aorta rings to high glucose (44 mmol/L) for 6 hours caused an inhibition of acetylcholine-induced endothelium-dependent relaxation but had no effect on sodium nitroprusside-induced endothelium-independent relaxation. Treatment with cariporide (0.01, 0.1, 1 micromol/L) of aortic rings incubated with high-glucose medium attenuated the impaired endothelium-dependent relaxation in a dose-dependent manner. Furthermore, high glucose resulted in an increase of malondialdehyde and a decrease of superoxide dismutase activity in rat aorta rings, and these effects were reversed by cariporide. In addition, cariporide was able to inhibit the activation of Na+/H+ exchanger induced by high glucose in cultured endothelial cells. These findings suggest that the endothelial dysfunction induced by high glucose in vitro is caused by the activation of Na+/H+ exchanger.
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