Geoffroy J, Benzoni D, Vincent M, Sassard J
Arch Mal Coeur Vaiss. 1986 Jun;79(6):864-6.
In order to assess the pathophysiological role of the renal Thromboxane (Tx)A2 in genetic hypertension, the urinary excretion of its stable metabolite: the TxB2 was followed in groups of 12 hypertensive (LH), normotensive (LN) and low blood pressure (LL) female rats of the Lyon strains at the ages of 5, 9, 21 and 32 weeks. In the 3 strains studied, the urinary TxB2 excretion markedly decreased between 5 and 9 weeks of age and did change thereafter. In addition, 5 and 9 weeks old rats exhibited an increased urinary TxB2 output compared to LN and LL controls. Since TxA2 is a potent vasoconstrictor, it seems likely to hypothesize that the early increase observed in the renal TxA2 biosynthesis could be one of the primary events occurring during the development of hypertension in this rat model.
为了评估肾血栓素（Tx）A2在遗传性高血压中的病理生理作用，在5、9、21和32周龄的里昂品系雌性大鼠中，分别对12只高血压（LH）、正常血压（LN）和低血压（LL）大鼠组的尿液中其稳定代谢产物血栓素B2（TxB2）的排泄情况进行了跟踪研究。在所研究的3个品系中，尿液TxB2排泄量在5至9周龄之间显著下降，之后没有变化。此外，与LN和LL对照组相比，5周龄和9周龄的大鼠尿液TxB2排出量增加。由于TxA2是一种强效血管收缩剂，因此可以推测，在该大鼠模型高血压发展过程中观察到的早期肾TxA2生物合成增加可能是主要事件之一。
