Reis M L, de Jesus W D, Bertramini-Sabbag L M, Krieger E M, Greene L J
Hypertension. 1984 Mar-Apr;6(2 Pt 1):255-61.
The present study was undertaken to evaluate the participation of the kallikrein-kinin system in the normalization of blood pressure after release of the clip in one-kidney, one clip hypertensive rats ( 1K1C ). Kininogen was determined before and after unclipping by tryptic digestion of denatured rat plasma, and spasmogenic activity was measured with isolated guinea pig ileum. In contrast to human plasma for which bradykinin (BK) is the only trypsin-releasable spasmogenic substance ( TRSS ), rat plasma contains non-BK TRSS (Fractions P1 and P2) as well as BK. Fractions P1 and P2 were separated from BK by SP-Sephadex chromatography. An increase of total TRSS was demonstrated 60 days after clipping and reached a maximum at approximately Day 75, which was two times that of the normotensive controls (NC). The level of total TRSS did not change after unclipping . The increased level of TRSS in the hypertensive state confirmed the observations of other investigators who reported increased kininogen levels but who could not distinguish between BK and non-BK TRSS because bioassays were performed without prior chromatographic separation of the spasmogenic activities. Fractions P1 and P2 were present in the TRSS of both 1K1C and NC plasma, but were two to six times higher in 1K1C and thus probably accounted quantitatively for the increased TRSS in 1K1C . The data suggest that in the hypertensive state there is an alteration in the relative amounts of some plasma proteins that contain non-BK TRSS within their amino acid sequences. Fractions P1 and P2 also contain potentiating peptides and have not yet been purified to homogeneity.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究旨在评估激肽释放酶 - 激肽系统在单肾单夹高血压大鼠（1K1C）夹闭解除后血压正常化过程中的作用。通过对变性大鼠血浆进行胰蛋白酶消化来测定夹闭解除前后的激肽原，并使用离体豚鼠回肠测量致痉活性。与人类血浆不同，人类血浆中缓激肽（BK）是唯一可被胰蛋白酶释放的致痉物质（TRSS），而大鼠血浆除了BK外还含有非BK的TRSS（组分P1和P2）。通过SP - 葡聚糖凝胶色谱法将组分P1和P2与BK分离。夹闭后60天总TRSS增加，并在大约第75天达到最大值，是正常血压对照组（NC）的两倍。夹闭解除后总TRSS水平未改变。高血压状态下TRSS水平的升高证实了其他研究者的观察结果，他们报告了激肽原水平升高，但由于在进行生物测定前未对致痉活性进行色谱分离，所以无法区分BK和非BK的TRSS。组分P1和P2存在于1K1C和NC血浆的TRSS中，但在1K1C中高出两到六倍，因此可能在数量上解释了1K1C中TRSS的增加。数据表明，在高血压状态下，一些氨基酸序列中含有非BK TRSS的血浆蛋白的相对含量发生了改变。组分P1和P2还含有增强肽，尚未纯化至同质状态。（摘要截断于250字）
