Girolami J P, Praddaude F, Bascands J L, Suc J M
Arch Mal Coeur Vaiss. 1984 Oct;77(11):1204-9.
Renal tissue kallikrein and proteins were measured in two kidney-one clip Goldblatt hypertensive rats both in the stenotic and the controlateral kidney and in sham operated rats at either 1 or 2 weeks after clipping. Activity was assessed by the amidolytic activity and by the kininogenase activity. Kallikrein in normotensive controls was 97.4 +/- 13 ng of bradykinin min-1 mg-1 of protein at week 1 and increased up to 116 +/- 18. Kallikrein in the GH rats was 83 +/- 12 in the stenotic kidney and 85,6 +/- 14 in the controlateral one at week 1, these values remained unchanged at week 2. As a consequence renal tissue kallikrein became significantly lower in the GH rats only at week 2 when compared to controls both the clipped and unclipped kidney showed the same magnitude decrease. Protein concentration remained at a steady level through out the 2 weeks of study. The results suggest that the lower renal kallikrein activity secondary to hypertension found in GH rats result from a decreased activation of prekallikrein in both kidney.
在夹闭肾动脉1周或2周后的双肾单夹型戈德布拉特高血压大鼠的狭窄肾和对侧肾以及假手术大鼠中，测定了肾组织激肽释放酶和蛋白质。通过酰胺水解活性和激肽原酶活性评估活性。正常血压对照组第1周的激肽释放酶为97.4±13 ng缓激肽·分钟⁻¹·毫克⁻¹蛋白质，第2周增加至116±18。戈德布拉特高血压大鼠第1周狭窄肾中的激肽释放酶为83±12，对侧肾为85.6±14，这些值在第2周保持不变。因此，仅在第2周时，与对照组相比，戈德布拉特高血压大鼠肾组织激肽释放酶显著降低，夹闭和未夹闭的肾均出现相同程度的降低。在整个2周的研究中，蛋白质浓度保持稳定水平。结果表明，戈德布拉特高血压大鼠中继发于高血压的较低肾激肽释放酶活性是由于双肾中前激肽释放酶的激活减少所致。
