Role of vasopressin in regulation of renal kinin excretion in Long-Evans and diabetes insipidus rats.
Role of vasopressin in regulation of renal kinin excretion in Long-Evans and diabetes insipidus rats.
复制标题
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
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Nasjletti,A
中科院分区：
文献类型：
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作者：
Kauker,ML;Crofton,JT;Share,L;Nasjletti,A
为了研究加压素与肾脏激肽释放酶-激肽系统的关系，我们测定了麻醉大鼠在加压素水平升高和降低的情况下，激肽排泄到尿液中的速率。患有遗传性尿崩症（DI）的Brattleboro大鼠（24 +/- 3 pg min-1 kg-1）的免疫反应性激肽分泌量低于对照Long Evans（LE）大鼠（182 +/- 22 pg min-1 kg-1; P <0.05）。DI大鼠还表现出可忽略的免疫反应性加压素的尿排泄，尿渗透压降低，尿流量和激肽原酶排泄增加。在LE大鼠中，通过输注0.45% NaCl-2.5%葡萄糖以降低血管加压素分泌的容量扩张使激肽排泄、血管加压素排泄和尿渗透压降低（P <0.05）至各自对照值的41%、26%和15%，同时增加（P <0.05）尿流量和激肽原酶排泄。另一方面，输注促进血管加压素分泌的5%NaCl使尿激肽和血管加压素的排泄量增加（P <0.05）至对照组的165和396%，同时增加尿流量和激肽原酶排泄量（P <0.05）。在用0.45%NaCl-2.5%葡萄糖扩容期间，血管加压素（1.2 mU/h，静脉注射）增强DI大鼠和LE大鼠的激肽排泄（P <0.05）2 - 3倍，同时减少尿流量和增加尿渗透压。这项研究表明，尿中分泌的免疫反应性激肽的变化与尿中加压素的水平有关，无论尿量和渗透压和尿中分泌的钠和激肽原酶。这项研究表明，加压素在促进大鼠肾脏激肽释放酶-激肽系统的活性中发挥作用。
To study the relationship between vasopressin and the renal kallikrein-kinin system we measured the rate of excretion of kinins into the urine of anesthetized rats during conditions of increased and decreased vasopressin level. The excretion of immunoreactive kinins in Brattleboro rats with hereditary diabetes insipidus (DI) (24 +/- 3 pg min-1 kg-1) was lower than in the control Long Evans (LE) rats (182 +/- 22 pg min-1 kg-1; P less than 0.05). The DI rats also exhibited negligible urinary excretion of immunoreactive vasopressin, reduced urine osmolality, and increased urine flow and kininogenase excretion. In LE rats, volume expansion by infusion of 0.45% NaCl-2.5% dextrose to lower vasopressin secretion reduced (P less than 0.05) kinin excretion, vasopressin excretion, and urine osmolality to 41, 26, and 15% of their respective control values, while increasing (P less than 0.05) urine flow and kininogenase excretion. On the other hand, the infusion of 5% NaCl, which promotes vasopressin secretion, increased (P less than 0.05) the urinary excretion of kinins and vasopressin to 165 and 396% of control, while increasing (P less than 0.05) urine flow and kininogenase excretion. Infusion of vasopressin (1.2 mU/h, intravenous) enhanced (P less than 0.05) kinin excretion by two to threefold in DI rats and in LE rats during volume expansion with 0.45% NaCl-2.5% dextrose, while decreasing urine flow and increasing urine osmolality. This study demonstrates that the urinary excretion of immunoreactive kinins varies in relation to the urinary level of vasopressin, irrespective of urine volume and osmolality and of the urinary excretions of sodium and kininogenase. The study suggests a role for vasopressin in promoting the activity of the renal kallikrein-kinin system in the rat.