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肾激肽释放酶在清醒大鼠肾素释放调控中的作用。

Role of renal kallikrein in control of renin release in conscious rats.

作者信息

Kobayashi M, Suzuki S, Hashiba K

出版信息

Am J Physiol. 1983 Mar;244(3):E262-5. doi: 10.1152/ajpendo.1983.244.3.E262.

Abstract

Renal kallikrein was reported to activate human inactive renin and to release active renin from rat renal cortical slices. To evaluate the role of renal kallikrein in the control of renin release in vivo, Trasylol and soybean trypsin inhibitor (SBTI) were used to determine whether they can inhibit renin release stimulated by the administration of furosemide and a 2-wk low-sodium diet. Plasma renin activity (PRA) was increased by furosemide and also by the low-sodium diet. Urinary kallikrein excretion was increased by the sodium depletions. Trasylol did not affect basal PRA; however, it inhibited PRA and urinary kallikrein excretion, when stimulated by furosemide and by a low-sodium diet. These results suggest that furosemide and low-sodium diet act on the kidney to release renin via protease production. Because SBTI affected neither PRA nor urinary kallikrein excretion stimulated by these sodium depletions, it is suggested that renal kallikrein may play an important role in the control of renin release stimulated by furosemide and by low-sodium diet.

摘要

据报道,肾激肽释放酶可激活人无活性肾素,并从大鼠肾皮质切片中释放活性肾素。为评估肾激肽释放酶在体内肾素释放调控中的作用,使用抑肽酶和大豆胰蛋白酶抑制剂(SBTI)来确定它们是否能抑制速尿和为期2周的低钠饮食所刺激的肾素释放。速尿和低钠饮食均可使血浆肾素活性(PRA)升高。钠缺乏可使尿激肽释放酶排泄增加。抑肽酶不影响基础PRA;然而,当受到速尿和低钠饮食刺激时,它可抑制PRA和尿激肽释放酶排泄。这些结果表明,速尿和低钠饮食通过蛋白酶生成作用于肾脏以释放肾素。由于SBTI对这些钠缺乏所刺激的PRA和尿激肽释放酶排泄均无影响,提示肾激肽释放酶可能在速尿和低钠饮食所刺激的肾素释放调控中起重要作用。

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