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。

Urinary kallikrein in the rat: stimulation with angiotensin infusion but depression with increasing sodium concentration.

作者信息

Mills I H, Lee G, Brownlee A A

机构信息

Department of Medicine, University of Cambridge, Addenbrooke's Hospital, UK.

出版信息

J Physiol. 1994 Dec 1;481 ( Pt 2)(Pt 2):425-37. doi: 10.1113/jphysiol.1994.sp020451.

DOI:10.1113/jphysiol.1994.sp020451

PMID:7738835

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1155941/

Abstract

The kallikrein response to angiotensin II infusion in the conscious rat was studied to compare it with the response in the dog. 2. Active kallikrein was measured by the aprotinin-suppressible esterase technique in 20 min periods. Angiotensin (5 x 10(-9) to 5 x 10(-2) micrograms min-1) was infused in 10 mM saline in period 10 (group A), or in 90 mM saline in periods 10-12 (group B). 3. In group A, no dose of angiotensin was antinatriuretic. Natriuresis and urinary sodium concentration were dose dependent. 4. Kallikrein excretion was dose dependent with angiotensin (P < 0.0001) and inversely correlated with urinary sodium concentration (P = 0.011). In natriuretic and non-natriuretic rats, kallikrein excretion after angiotensin was inversely correlated with urinary sodium concentration in the preceding period. 5. In group B, natriuresis and urinary sodium concentration were dose dependent. Kallikrein excretion in periods 10-13 was inversely correlated with urinary sodium concentration in the preceding period (P = 0.0001) and inversely correlated with urinary osmolality in periods 9-13. 6. Infusion of angiotensin II at 5 x 10(-6) micrograms min-1 led to antinatriuresis. 7. Formulae were derived which enabled the opposing effects of angiotensin and urinary sodium concentration on kallikrein excretion to be separated. In group A both these effects were statistically significant only in the natriuretic rats (natriuresis > 20 mumols per period). In group B the formulae showed a dose-dependent rise in kallikrein excretion, which was counteracted by the decrease in kallikrein excretion associated with the increasing urinary sodium concentration. 8. With infusions of 0.9% saline, kallikrein excretion in periods 10-13 was inversely correlated with urinary sodium concentration in the preceding period (P = 0.001). 9. The overall effect in the rat differs from that in the dog, where kallikrein increases with angiotensin natriuresis and dilution of the urine occurs.

摘要

研究清醒大鼠中激肽释放酶对输注血管紧张素II的反应，以与犬的反应进行比较。2. 采用抑肽酶抑制的酯酶技术，在20分钟时间段内测量活性激肽释放酶。在第10期（A组），血管紧张素（5×10⁻⁹至5×10⁻²微克·分钟⁻¹）以10 mM盐水输注，或在第10 - 12期（B组）以90 mM盐水输注。3. 在A组中，没有剂量的血管紧张素具有抗利尿钠作用。利尿钠作用和尿钠浓度呈剂量依赖性。4. 激肽释放酶排泄与血管紧张素呈剂量依赖性（P < 0.0001），且与尿钠浓度呈负相关（P = 0.011）。在利尿钠和非利尿钠大鼠中，血管紧张素后的激肽释放酶排泄与前一时期的尿钠浓度呈负相关。5. 在B组中，利尿钠作用和尿钠浓度呈剂量依赖性。第10 - 13期的激肽释放酶排泄与前一时期的尿钠浓度呈负相关（P = 0.0001），且与第9 - 13期的尿渗透压呈负相关。6. 以5×10⁻⁶微克·分钟⁻¹的速率输注血管紧张素II导致抗利尿钠作用。7. 推导了公式，能够区分血管紧张素和尿钠浓度对激肽释放酶排泄的相反作用。在A组中，仅在利尿钠大鼠（每期利尿钠> 20微摩尔）中，这两种作用在统计学上均显著。在B组中，公式显示激肽释放酶排泄呈剂量依赖性升高，但与尿钠浓度增加相关的激肽释放酶排泄减少抵消了这种升高。8. 输注0.9%盐水时，第10 - 13期的激肽释放酶排泄与前一时期的尿钠浓度呈负相关（P = 0.001）。9. 大鼠中的总体效应与犬不同，在犬中，激肽释放酶随血管紧张素利尿钠作用增加，且尿液发生稀释。