Abebe Worku, Mozaffari Mahmood S
Department of Oral Biology and Maxillofacial Pathology, CB 3710, School of Dentistry, Medical College of Georgia, Augusta, GA 30912-1128, USA.
Can J Physiol Pharmacol. 2003 Sep;81(9):903-9. doi: 10.1139/y03-088.
We recently showed that chronic taurine supplementation is associated with attenuation of contractile responses of rat aorta to norepinephrine and potassium chloride. However, the potential involvement of endogenous taurine in modulation of vascular reactivity is not known. Therefore, we examined the effect of beta-alanine-induced taurine depletion on the in vitro reactivity of rat aorta to selected vasoactive agents. The data indicate that both norepinephrine- and potassium-chloride-induced maximum contractile responses of endothelium-denuded aortae were enhanced in taurine-depleted rats compared with control animals. However, taurine depletion did not affect tissue sensitivity to either norepinephrine or potassium chloride. By contrast, sensitivity of the endothelium-denuded aortae to sodium nitroprusside was attenuated by taurine depletion. Similarly, taurine deficiency reduced the relaxant responses of endothelium-intact aortic rings elicited by submaximal concentrations of acetylcholine, and this effect was associated with decreased nitric oxide production. Taken together, the data suggest that taurine depletion augments contractility but attenuates relaxation of vascular smooth muscle in a nonspecific manner. Impairment of endothelium-dependent responses, which is at least in part associated with reduced nitric oxide generation, may contribute to the attenuation of the vasorelaxant responses. These vascular alterations could be of potential consequence in pathological conditions associated with taurine deficiency.
我们最近发现，长期补充牛磺酸与大鼠主动脉对去甲肾上腺素和氯化钾的收缩反应减弱有关。然而，内源性牛磺酸在调节血管反应性中的潜在作用尚不清楚。因此，我们研究了β-丙氨酸诱导的牛磺酸耗竭对大鼠主动脉对选定血管活性药物的体外反应性的影响。数据表明，与对照动物相比，牛磺酸耗竭的大鼠中去甲肾上腺素和氯化钾诱导的内皮剥脱主动脉的最大收缩反应增强。然而，牛磺酸耗竭并不影响组织对去甲肾上腺素或氯化钾的敏感性。相比之下，牛磺酸耗竭减弱了内皮剥脱主动脉对硝普钠的敏感性。同样，牛磺酸缺乏降低了亚最大浓度乙酰胆碱引起的内皮完整主动脉环的舒张反应，并且这种作用与一氧化氮生成减少有关。综上所述，数据表明牛磺酸耗竭以非特异性方式增强了血管平滑肌的收缩性但减弱了其舒张性。内皮依赖性反应的受损，至少部分与一氧化氮生成减少有关，可能导致血管舒张反应减弱。这些血管改变在与牛磺酸缺乏相关的病理状况中可能具有潜在影响。
