Diabetes affects millions of people worldwide. This devastating disease dramatically increases the risk of developing cardiovascular disorders. A hallmark metabolic abnormality in diabetes is hyperglycemia, which contributes to the pathogenesis of cardiovascular complications. These cardiovascular complications are, at least in part, related to hyperglycemia-induced molecular and cellular changes in the cells making up blood vessels. Whereas the mechanisms mediating endothelial dysfunction during hyperglycemia have been extensively examined, much less is known about how hyperglycemia impacts vascular smooth muscle function. Vascular smooth muscle function is exquisitely regulated by many ion channels, including several members of the potassium (K⁺) channel superfamily and voltage-gated L-type Ca²⁺ channels. Modulation of vascular smooth muscle ion channels function by hyperglycemia is emerging as a key contributor to vascular dysfunction in diabetes. In this review, we summarize the current understanding of how diabetic hyperglycemia modulates the activity of these ion channels in vascular smooth muscle. We examine underlying mechanisms, general properties, and physiological relevance in the context of myogenic tone and vascular reactivity.

糖尿病影响着全世界数百万人。这种毁灭性的疾病极大地增加了患心血管疾病的风险。糖尿病的一个标志性代谢异常是高血糖，它导致心血管并发症的发病机制。这些心血管并发症至少部分与高血糖引起的构成血管的细胞的分子和细胞变化有关。尽管高血糖期间介导内皮功能障碍的机制已被广泛研究，但人们对高血糖如何影响血管平滑肌功能知之甚少。血管平滑肌功能受到许多离子通道的精细调节，包括钾 (K ⁺ ) 通道超家族的几个成员和电压门控 L 型 Ca ²⁺通道。高血糖对血管平滑肌离子通道功能的调节正在成为糖尿病血管功能障碍的关键因素。在这篇综述中，我们总结了目前对糖尿病高血糖如何调节血管平滑肌中这些离子通道活性的理解。我们在肌源张力和血管反应性的背景下研究潜在机制、一般特性和生理相关性。