Beltramini-Sabbag L M, Izumi C, Greene L J
Departamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Brasil.
Braz J Med Biol Res. 1988;21(3):457-60.
We measured the levels of trypsin-releasable spasmogenic substances (TRSS) in the plasma of spontaneously hypertensive rats (SHR) during the development of hypertension. TRSS levels (means +/- SEM, N = 4) were significantly higher at 12 weeks (7.13 +/- 1.05 micrograms bradykinin equivalents (BKE)/ml plasma) and 24 weeks (6.87 +/- 0.60 micrograms BKE/ml) compared to 8 weeks (3.3 +/- 0.55 micrograms BKE/ml) and to normotensive Wistar Kyoto (WKN) rats, whose levels were 3.74 +/- 0.74 micrograms BKE/ml at 24 weeks and did not change significantly during the period studied. The mean arterial pressure (MAP) of SHR was 150-170, 160-180 and 170-220 mmHg at 8, 12 and 24 weeks, respectively, whereas the WKN MAP was 110-120 mmHg at 24 weeks. The increase in total TRSS was due to substances which elicit the slow contraction of the isolated guinea pig ileum and which could be distinguished from BK, T-kinin and other BK homologues by gel filtration on Sephadex G-25, gradient elution chromatography on CM-cellulose and by the slow rate of contraction of the guinea pig ileum. All of these properties are the same as those we have previously demonstrated for TRSS of Goldblatt 1-kidney 1-clip renal hypertensive rats and which are due, at least in part, to a 14 amino acid peptide whose composition does not correspond to any known spasmogenic substance.
我们测量了自发性高血压大鼠(SHR)在高血压发展过程中血浆中胰蛋白酶可释放的致痉挛物质(TRSS)的水平。与8周龄时(3.3±0.55微克缓激肽当量(BKE)/毫升血浆)以及正常血压的Wistar Kyoto(WKN)大鼠相比,SHR在12周龄时(7.13±1.05微克BKE/毫升血浆)和24周龄时(6.87±0.60微克BKE/毫升)的TRSS水平(平均值±标准误,N = 4)显著更高,WKN大鼠在24周龄时的TRSS水平为3.74±0.74微克BKE/毫升,并且在研究期间没有显著变化。SHR在8周龄、12周龄和24周龄时的平均动脉压(MAP)分别为150 - 170 mmHg、160 - 180 mmHg和170 - 220 mmHg,而WKN大鼠在24周龄时的MAP为110 - 120 mmHg。总TRSS的增加是由于能引起豚鼠离体回肠缓慢收缩的物质导致的,这些物质通过在Sephadex G - 25上的凝胶过滤、在CM - 纤维素上的梯度洗脱色谱以及豚鼠回肠缓慢的收缩速率,可与缓激肽、T - 激肽和其他缓激肽同源物区分开来。所有这些特性与我们之前对Goldblatt 1肾1夹肾性高血压大鼠的TRSS所证明的特性相同,并且至少部分是由于一种14氨基酸肽导致的,其组成与任何已知的致痉挛物质都不对应。