Abstract：
Bradykinin has a wide variety of physiological functions, including vasodilation and blood pressure reduction. However, the physiological roles of bradykinin are not fully understood. We used the CRISPR/Cas9 method to generate BKdelK1 and BKdelK2 mutant mice, targeting the BK portion of mouse kininogen1 and kininogen2 genes, respectively. The BKdelK1 and BKdelK2 mutant mice had about 50% reductions in plasma low molecular weight kininogen and trypsin-released BK, compared to wild mice. Both BKdelK1 and BKdelK2 mice had significantly elevated systolic blood pressure compared to WT mice. These results suggest that plasma LKNG is a source of KNG in the vascular kallikrein-kinin system and contributes to maintaining lower systolic blood pressure.
摘要：
缓激肽具有多种生理功能,包括血管舒张和血压降低.然而,缓激肽的生理作用尚不完全清楚。我们使用CRISPR/Cas9方法产生BKdelK1和BKdelK2突变小鼠，靶向小鼠激肽原1和激肽原2基因的BK部分，分别。BKdelK1和BKdelK2突变小鼠的血浆低分子量激肽原和胰蛋白酶释放的BK减少了约50％，与野生老鼠相比。与WT小鼠相比,BKdelK1和BKdelK2小鼠均具有显著升高的收缩压。这些结果表明，血浆LKNG是血管激肽释放酶激肽系统中KNG的来源，有助于维持较低的收缩压。
