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Effects of taurine on the reactivity of aortas from diabetic rats

机译：牛磺酸对糖尿病大鼠主动脉反应性的影响

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The effects of the semi-essential amino acid-like nutrient, taurine, on alterations in the reactivities of aortas from male rats with chronic streptozotocin-induced diabetes were examined under in vitro conditions. In the absence of taurine, the contractile responsiveness of endothelium-denuded aortic rings from diabetic rats to norepinephrine, but not KCl, was enhanced compared to controls. This effect of norepinephrine on the diabetic rat aorta appeared to be associated with increased release of intracellular calcium, influx of extracellular calcium and protein kinase C-mediated responses. Incubation of endothelium-denuded aortic rings with 10 mM, but not 5 mM, taurine for 2 h reduced the augmented contractile responses of the tissues from diabetic rats to norepinephrine close to control levels, and this was associated with inhibition of responses linked to the release and influx of calcium, and protein kinase C activation. Endothelium-dependent relaxation of aortas from diabetic rats to acetylcholine was depressed relative to controls. This effect of diabetes was ameliorated close to control levels by incubating the tissues with 10 mM, but not 5 mM, taurine for 2 h. Incubation of nondiabetic rat aortic rings with 45 mM glucose for 3 h caused enhancement of contraction of the vascular smooth muscle to phenylephrine and impairment of endothelium-mediated vasorelaxation to acetylcholine, as compared to control responses. Co-incubation of the tissues with 5-10 mM taurine concentration-dependently reduced the alterations in both contractile and relaxant responses caused by high glucose. Overall, the data suggest that taurine ameliorates or prevents vascular reactivity alterations in diabetes. Such an observation provides preliminary evidence for taurine's potential as a therapeutic agent for the prevention or amelioration of vascular disorders in diabetes. (C) 2007 Elsevier Inc. All rights reserved.
机译：在体外条件下，研究了半必需氨基酸样营养物质牛磺酸对慢性链脲佐菌素诱发的糖尿病雄性大鼠主动脉反应性改变的影响。在没有牛磺酸的情况下，与对照组相比，糖尿病大鼠对内皮去甲肾上腺环的去甲肾上腺素而不是氯化钾的收缩反应性增强。去甲肾上腺素对糖尿病大鼠主动脉的这种作用似乎与细胞内钙的释放增加，细胞外钙的流入和蛋白激酶C介导的反应有关。用10 mM但不是5 mM的牛磺酸孵育内皮剥落的主动脉环2小时，使糖尿病大鼠对去甲肾上腺素的组织收缩反应增强，接近对照水平，这与抑制与释放相关的反应有关钙的流入和蛋白激酶C的活化相对于对照，从糖尿病大鼠到乙酰胆碱的内皮依赖性的主动脉松弛被抑制。通过将牛磺酸与10 mM（而不是5 mM）组织孵育2 h，可以使糖尿病的这种影响接近对照水平，从而得到改善。与对照反应相比，将非糖尿病大鼠主动脉环与45 mM葡萄糖一起孵育3 h会导致血管平滑肌向去氧肾上腺素的收缩增强，并使内皮介导的血管舒张减弱为乙酰胆碱。用浓度为5-10 mM的牛磺酸共同孵育组织可减少高葡萄糖引起的收缩反应和松弛反应的变化。总体而言，数据表明牛磺酸可改善或预防糖尿病中血管反应性的改变。这样的观察为牛磺酸作为预防或改善糖尿病血管疾病的治疗剂的潜力提供了初步证据。 （C）2007 Elsevier Inc.保留所有权利。

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