Bompart G, Collé A, Dos Reiss M L, Pécher C, Adam A, Girolami J P
INSERM U133, Centre de Recherche Louis Bugnard, Faculté de Médecine Rangueil, Toulouse, France.
Nephron. 1993;65(4):612-8. doi: 10.1159/000187573.
In the present study, we investigated the plasma, urinary and intrarenal concentrations of low and high molecular weight kininogens during sodium chromate (25 mg/kg body weight)-induced acute renal failure (ARF) in the rat. Urinary kininogen underwent a transient increase with a maximum on day 7 (78 +/- 22 versus 4.2 +/- 1.6 ng bradykinin/mg creatinine) whereas plasma kininogen did not and glomerular filtration rate decreased (92 +/- 8 versus 895 +/- 70 microliters/min). The tissue level of kininogen was enhanced both in the cortex (1,319 +/- 123 versus 86 +/- 8 pg bradykinin Eq/mg protein) and in the medulla (1,673 +/- 138 versus 44 +/- 9 pg bradykinin Eq/mg protein) but more in the medulla (36 +/- 4- versus 15 +/- 3-fold). As plasma kininogen level was unchanged and glomerular filtration rate decreased, the increase in both renal concentration and urinary excretion of kininogen probably reflects stimulated renal production of kininogen in this model of ARF. Whether the evoked renal production of kininogen results from a local inflammatory response only or may subserve another physiological purpose remains to be elucidated.
在本研究中，我们调查了大鼠在重铬酸钠（25毫克/千克体重）诱导的急性肾衰竭（ARF）过程中，血浆、尿液和肾内低分子量及高分子量激肽原的浓度。尿激肽原出现短暂升高，在第7天达到峰值（78±22对4.2±1.6纳克缓激肽/毫克肌酐），而血浆激肽原未升高，肾小球滤过率下降（92±8对895±70微升/分钟）。激肽原的组织水平在皮质（1319±123对86±8皮克缓激肽当量/毫克蛋白质）和髓质（1673±138对44±9皮克缓激肽当量/毫克蛋白质）均升高，但在髓质升高更多（36±4对15±3倍）。由于血浆激肽原水平未变而肾小球滤过率下降，激肽原在肾脏浓度和尿排泄的增加可能反映了在该急性肾衰竭模型中肾脏激肽原生成受到刺激。肾脏激肽原的诱导生成是仅由局部炎症反应引起，还是可能有其他生理作用，仍有待阐明。
