Bressler R, Grosso D S, Roeske W R
Trans Assoc Am Physicians. 1977;90:257-69.
Myocardial taurine concentrations have been found to be elevated in hypertension and congestive heart failure states in animals and humans. The mechanism(s) by which myocardial taurine levels increase isn't known. Biosynthesis of taurine by the heart has not been established as a significant process. The fetal mouse heart in culture was used to characterize a taurine uptake system. The uptake of taurine was found to be saturable, temperature and sodium dependent and inhibited by close structural analogs. Taurine uptake was energy dependent and accumulated taurine against a concentration gradient indicating that taurine transport is an active process. Failure of alpha-alanine, alpha-aminoisobutyric acid, glycine, leucine or threonine to decrease taurine uptake establishes that the taurine uptake system is separate and distinct from other neutral alpha-amino acid transport systems in the heart.
在动物和人类中,已发现高血压和充血性心力衰竭状态下心肌中的牛磺酸浓度会升高。心肌牛磺酸水平升高的机制尚不清楚。心脏合成牛磺酸尚未被确认为一个重要过程。利用培养的胎鼠心脏来表征牛磺酸摄取系统。发现牛磺酸的摄取是可饱和的,依赖温度和钠,并受到结构类似物的抑制。牛磺酸摄取依赖能量,并能逆浓度梯度积累牛磺酸,这表明牛磺酸转运是一个主动过程。α-丙氨酸、α-氨基异丁酸、甘氨酸、亮氨酸或苏氨酸不能降低牛磺酸摄取,这表明牛磺酸摄取系统与心脏中其他中性α-氨基酸转运系统是分开且不同的。