Urinary Kallikrein Excretion in Normal Man: Relationships to Sodium Intake and Sodium‐Retaining Steroids
Urinary Kallikrein Excretion in Normal Man: Relationships to Sodium Intake and Sodium‐Retaining Steroids
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正常人尿激肽释放酶排泄：与钠摄入量和钠保留类固醇的关系
DOI：
10.1161/01.res.35.6.812
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发表时间：
1974
影响因子：
20.1
通讯作者：
H. Keiser
中科院分区：
文献类型：
--
作者：
H. Margolius;D. Horwitz;R. Geller;R. Alexander;J. Gill;J. Pisano;H. Keiser
尿中排泄的激肽释放酶，肾酶切割的有效的血管扩张剂激肽，胰激肽，从激肽原，测量正常志愿者通过三种不同的测定，其中之一是生物测定。当钠摄入量从随意或109 mEq/天变为9 mEq/天时，每例受试者的每日激肽释放酶排泄量逐渐增加，至第7天达到平均最大值，为对照组的271%;钠摄入量增加至259 mEq/天导致激肽释放酶排泄量恢复至对照值。尿中淀粉酶（一种分子量与激肽释放酶相似的蛋白质）的排泄量在钠摄入量改变时没有改变，但血浆肾素活性和醛固酮排泄量相应改变。在接受恒定钠（109 mEq/天）、恒定钾（100 mEq/天）饮食的受试者中，氟氢可的松0.5 mg/天，持续10天，使激肽释放酶排泄增加至平均最大值，为对照组的203%。在饮食中含9 mEq钠/天的受试者中，在螺内酯400 mg/天治疗期间，激肽释放酶排泄升高降低。快速饮水（30分钟内1或2升，口服）或快速输注2.4升生理盐水，尽管尿量或钠排泄量发生较大变化，但未显著改变尿激肽释放酶排泄。因此，激肽释放酶排泄似乎与循环钠保留类固醇的有效水平直接相关。这些发现与激肽释放酶-激肽系统在肾脏对钠保留激素的反应中的作用一致。
The urinary excretion of kallikrein, a renal enzyme that cleaves the potent vasodilator kinin, kallidin, from kininogen, was measured in normal volunteers by three different assays, one of which was a bioassay. When sodium intake was changed from ad libitum or 109 mEq/day to 9 mEq/day, daily kallikrein excretion increased progressively in every subject to a mean maximal value that was 271% of control by day 7; an increase in sodium intake to 259 mEq/day resulted in the return of kallikrein excretion to control values. Urinary excretion of amylase, a protein with a molecular weight similar to that of kallikrein, did not change when sodium intake was changed, but plasma renin activity and aldosterone excretion changed appropriately. In subjects on a constant-sodium (109 mEq/day), constant-potassium (100 mEq/day) diet, fludrocortisone, 0.5 mg/day for 10 days, increased kallikrein excretion to a mean maximal value that was 203% of control. In subjects on a diet containing 9 mEq sodium/day, elevated kallikrein excretion decreased during treatment with spironolactone, 400 mg/day. Rapid administration of water (1 or 2 liters in 30 minutes, orally) or rapid infusion of 2.4 liters of normal saline did not significantly alter urinary kallikrein excretion despite large changes in urine volume or sodium excretion. Thus, kallikrein excretion appears to be directly related to the effective level of circulating sodium-retaining steroid. The findings are consistent with a role for the kallikrein-kinin system in the renal response to sodium-retaining hormones.