Garcia R, Thibault G, Genest J
Am J Physiol. 1984 Jul;247(1 Pt 2):R29-33. doi: 10.1152/ajpregu.1984.247.1.R29.
In pentobarbital-anesthetized rats the lymphatic vessels next to the renal artery and the urinary bladder were cannulated and lymph and urine were collected for 3 h. The kidneys were then washed and removed. Four experimental groups were studied. Kallikrein was measured in lymph, urine, and kidney extracts by a direct radioimmunoassay. Immunoreactive renal and urinary kallikreins were higher in a Na-deficient group. No changes were brought about by furosemide administration or Na supplementation. A very low concentration of immunoreactive kallikrein was found in lymph, with no differences between the groups. In the same urine and kidney extract samples, both total (trypsin-activated) kallikrein and naturally active kallikrein were determined as kininogenase activity in the rat uterus bioassay. Both active and inactive kallikreins were found in kidney and urine, but most of the changes induced by a Na-deficient diet or furosemide administration were restricted to the active form. It is suggested that the lymphatic route in the kidney is probably not an important source of circulating immunoreactive glandular kallikrein.
在戊巴比妥麻醉的大鼠中,将肾动脉和膀胱旁的淋巴管插管,并收集淋巴液和尿液3小时。然后冲洗并摘除肾脏。研究了四个实验组。通过直接放射免疫测定法测定淋巴液、尿液和肾脏提取物中的激肽释放酶。缺钠组的免疫反应性肾和尿激肽释放酶较高。给予呋塞米或补充钠均未引起变化。在淋巴液中发现免疫反应性激肽释放酶的浓度非常低,各组之间无差异。在相同的尿液和肾脏提取物样本中,通过大鼠子宫生物测定法将总(胰蛋白酶激活)激肽释放酶和天然活性激肽释放酶都测定为激肽原酶活性。在肾脏和尿液中都发现了活性和非活性激肽释放酶,但缺钠饮食或给予呋塞米引起的大多数变化仅限于活性形式。提示肾脏中的淋巴途径可能不是循环免疫反应性腺激肽释放酶的重要来源。