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大鼠尿激肽释放酶活性与盐和水排泄的分离

Dissociation of urinary kallikrein activity and salt and water excretion in the rat.

作者信息

Pollock D M, Butterfield M I, Ader J L, Arendshorst W J

出版信息

Am J Physiol. 1986 Jun;250(6 Pt 2):F1082-9. doi: 10.1152/ajprenal.1986.250.6.F1082.

DOI:10.1152/ajprenal.1986.250.6.F1082
PMID:2424322
Abstract

Experiments were designed to examine the relationship, if any, between urinary kallikrein activity (amidolytic assay) and sodium and water excretion in 12-wk-old Munich-Wistar rats. Five groups of animals were studied: euvolemic, saline-expanded and water-loaded anesthetized rats, and euvolemic and saline-expanded conscious restrained rats. Following surgery, animals were allowed to stabilize (60-180 min) and reach a steady-state urine flow. By design, basal sodium and/or water excretion varied markedly among groups as a function of hydration state. Group means for sodium excretion and urine flow ranged from 0.8 to 12.4 mu eq/min and 6 to 112 microliter/min, respectively. In contrast, neither active nor total urinary kallikrein activity differed significantly among the five groups. In anesthetized euvolemic rats, intravenous administration of aprotinin produced a dose-dependent decrease in urinary kallikrein activity. The greatest inhibition of 93 +/- 3% (active) and 72 +/- 10% (total) was observed with a dose of 5,000 kallikrein inhibiting units (KIU)/kg and 1,000 KIU X kg-1 X min-1. This dose produced a significant decrease in active and total kallikrein activity in each group (P less than 0.001). However, sodium and water excretion were unchanged in aprotinin-treated rats and similar to values in vehicle-treated time-control groups. Linear regression analysis revealed no significant correlations between urinary kallikrein activity and sodium excretion or urine flow either among or within groups. These results indicate that urinary kallikrein activity is not related to acute sodium and water homeostasis in anesthetized or conscious rats.

摘要

设计实验以研究12周龄慕尼黑-威斯塔大鼠尿激肽释放酶活性(酰胺水解测定法)与钠和水排泄之间的关系(若存在关系的话)。研究了五组动物:血容量正常、盐水扩容和水负荷的麻醉大鼠,以及血容量正常和盐水扩容的清醒束缚大鼠。手术后,让动物稳定(60 - 180分钟)并达到稳定的尿流状态。按照设计,基础钠和/或水排泄在各实验组之间因水合状态的不同而有显著差异。钠排泄和尿流的组均值分别为0.8至12.4微当量/分钟和6至112微升/分钟。相比之下,五组之间的活性尿激肽释放酶活性和总尿激肽释放酶活性均无显著差异。在麻醉的血容量正常大鼠中,静脉注射抑肽酶会使尿激肽释放酶活性呈剂量依赖性降低。在剂量为5000激肽释放酶抑制单位(KIU)/千克和1000 KIU×千克⁻¹×分钟⁻¹时,观察到最大抑制率分别为93±3%(活性)和72±10%(总活性)。该剂量使每组的活性和总激肽释放酶活性均显著降低(P < 0.001)。然而,抑肽酶处理的大鼠的钠和水排泄未发生变化,且与载体处理的时间对照组的值相似。线性回归分析显示,无论是在组间还是组内,尿激肽释放酶活性与钠排泄或尿流之间均无显著相关性。这些结果表明,在麻醉或清醒大鼠中,尿激肽释放酶活性与急性钠和水平衡无关。

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Dissociation of urinary kallikrein activity and salt and water excretion in the rat.大鼠尿激肽释放酶活性与盐和水排泄的分离
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The influence of isotonic saline administration on the urinary excretion of kallikrein in rats.
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Urinary kallikrein in the rat: stimulation with angiotensin infusion but depression with increasing sodium concentration.
大鼠尿激肽释放酶:血管紧张素输注可刺激其分泌,但随着钠浓度升高其分泌受到抑制。
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Klin Wochenschr. 1988 Sep 15;66(18):849-56. doi: 10.1007/BF01728946.