High sensitivity to salt in kininogen-deficient brown Norway Katholiek rats.
High sensitivity to salt in kininogen-deficient brown Norway Katholiek rats.
复制标题
缺乏激肽原的棕色挪威 Katholiek 大鼠对盐高度敏感。
作者：
M. Majima;O. Yoshida;H. Mihara;T. Muto;S. Mizogami;Y. Kuribayashi;M. Katori;S. Oh‐ishi
棕色挪威Katholiek大鼠的血浆激肽原水平非常低，与同一品系的正常大鼠相比，它们在尿液中排出的激肽量要少得多。低（0.3%）NaCl （131 +/- 4 mm Hg, n = 12）喂养的7周龄激肽原缺乏大鼠的收缩压与正常大鼠无显著差异。从7周龄开始，连续4周给予2% NaCl的饮食，导致缺陷大鼠的血压迅速升高（167 +/- 4毫米汞柱，n = 12,9周龄），尽管同样的饮食不会引起正常大鼠的血压升高。在整个NaCl加载过程中，两组大鼠尿中活性钾化酶和原钾化酶的排泄量保持不变。在此期间，缺陷大鼠尿分泌减少（9周龄，P < 0.05），尿钠分泌减少（11周龄，P < 0.05）。9周龄时，钠缺乏大鼠血清钠水平高于正常大鼠（P < 0.05）。在整个NaCl加载过程中，钠缺陷大鼠红细胞内钠浓度高于正常大鼠（P < 0.05）。用渗透泵皮下输注牛低分子激肽原可使低盐钠血症大鼠血压降低（P < 0.01），尿量、尿钠和激肽水平升高（P < 0.05）。相比之下，在正常大鼠中皮下输注缓激肽拮抗剂ho140或抑肽酶可诱导高血压反应。这种拮抗剂治疗减少了尿量和尿钠。这些结果表明，激肽原缺乏的大鼠体内激肽的生成与钠潴留和NaCl负荷引起的高血压反应有关。
Brown Norway Katholiek rats, which have very low levels of plasma kininogens, excreted a much smaller amount of kinin in the urine than normal rats of the same strain. The systolic blood pressure of 7-week-old kininogen-deficient rats fed low (0.3%) NaCl diets (131 +/- 4 mm Hg, n = 12) was not different from that in normal rats. Two percent NaCl diets given from 7 weeks of age for 4 weeks caused rapid increases in blood pressure (167 +/- 4 mm Hg, n = 12, 9 weeks old) in deficient rats, although the same diets induced no blood pressure increase in normal rats. Urinary excretion of active kallikrein and prokallikrein remained constant in both rat groups throughout NaCl loading. During this period, the deficient rats secreted less urine (9 weeks old, P < .05) and less urinary sodium (11 weeks old, P < .05). Serum levels of sodium in deficient rats were higher (P < .05) than in normal rats at 9 weeks of age. Intracellular concentrations of sodium in the erythrocytes of deficient rats were higher (P < .05) than in normal rats throughout NaCl loading. Subcutaneous infusion of bovine low molecular weight kininogen with an osmotic pump in NaCl-loaded deficient rats induced a reduction (P < .01) in blood pressure and increases (P < .05) in urine volume and urinary sodium and kinin levels. By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 or of aprotinin in NaCl-loaded normal rats induced a hypertensive response. This antagonist treatment reduced urine volume and urinary sodium. These results indicate that the lack of kinin generation observed in the kininogen-deficient rats was related through sodium retention to the hypertensive response to NaCl loading.
加压素在调节 Long-Evans 和尿崩症大鼠肾激肽排泄中的作用。
DOI：
10.1172/jci111277
发表时间：
1984
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Kauker,ML;Crofton,JT;Share,L;Nasjletti,A
通讯作者：
Nasjletti,A
人尿无活性激肽释放酶（前激肽释放酶）的测定方法。
DOI：
10.1620/tjem.137.269
发表时间：
1982
期刊：
The Tohoku journal of experimental medicine
影响因子：
--
作者：
Shimamoto,K;Chao,J;Margolius,HS
通讯作者：
Margolius,HS