首页> 外文期刊>Endothelium: Journal of endothelial cell research >Mediation of vascular relaxation in epineurial arterioles of the sciatic nerve: effect of diabetes in type 1 and type 2 diabetic rat models.
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Mediation of vascular relaxation in epineurial arterioles of the sciatic nerve: effect of diabetes in type 1 and type 2 diabetic rat models.

机译:坐骨神经海马小动脉中血管舒张的介导:糖尿病在1型和2型糖尿病大鼠模型中的作用。

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Previously, the authors have reported that acetylcholine-induced vascular relaxation in epineurial arterioles of the sciatic nerve is mediated by nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Furthermore, they have demonstrated that acetylcholine-induced vasodilation in these vessels is impaired in streptozotocin-induced (type 1) and ZDF obese (type 2) diabetic rats. In the present study, the authors sought to determine the effect of diabetes on NO- and EDHF-mediated vasodilation in epineurial arterioles. In epineurial arterioles from nondiabetic Sprague-Dawley rats, NO and EDHF are equivalent in regard to their contribution to acetylcholine-induced vascular relaxation. In contrast, NO accounts for a greater portion of acetylcholine-induced vascular relaxation in normal glycemic ZDF lean rats. Following 4 weeks of hyperglycemia, the EDHF component of acetylcholine-induced vascular relaxation was totally inhibited in both streptozotocin-induced and ZDF obese diabetic rats. Vasodilation mediated by NO was still active in epineurial arterioles from both type 1 and type 2 diabetic rat models. These data suggest that diabetes causes an impairment in EDHF-mediated vascular relaxation and that interventions directed at improving EDHF production or bioactivity may improve vascular function in epineurial arterioles in diabetes.
机译:以前,作者已经报告说,一氧化氮(NO)和内皮源性超极化因子(EDHF)介导了乙酰胆碱诱导的坐骨神经小神经小动脉血管舒张。此外,他们已证明,在链脲佐菌素诱导的(1型)和ZDF肥胖(2型)糖尿病大鼠中,乙酰胆碱诱导的这些血管的血管舒张功能受损。在本研究中,作者试图确定糖尿病对肾小管小动脉中NO和EDHF介导的血管舒张的影响。在非糖尿病Sprague-Dawley大鼠的肾小管小动脉中,NO和EDHF对乙酰胆碱引起的血管舒张的贡献相同。相反,在正常的ZDF瘦身大鼠中,NO占乙酰胆碱诱导的血管舒张的更大部分。高血糖4周后,在链脲佐菌素诱导的和ZDF肥胖的糖尿病大鼠中,乙酰胆碱诱导的血管舒张的EDHF成分均被完全抑制。在1型和2型糖尿病大鼠模型的海马小动脉中,NO介导的血管舒张作用仍然活跃。这些数据表明,糖尿病会导致EDHF介导的血管舒张功能受损,并且针对改善EDHF产生或生物活性的干预措施可能会改善糖尿病患者肾小管小动脉的血管功能。

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