首页> 美国卫生研究院文献>The Journal of Physiology >Urinary kallikrein in the rat: stimulation with angiotensin infusion but depression with increasing sodium concentration.
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Urinary kallikrein in the rat: stimulation with angiotensin infusion but depression with increasing sodium concentration.

机译:大鼠尿激肽释放酶:通过血管紧张素输注刺激但随着钠浓度增加而降低。

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摘要

1. 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.
机译:1.研究了激肽释放酶对清醒大鼠对血管紧张素II输注的反应,并将其与狗的反应进行了比较。 2.通过抑肽酶抑制性酯酶技术在20分钟内测量活性激肽释放酶。在第10期(A组)中将血管紧张素(5 x 10(-9)至5 x 10(-2)微克min-1)注入10 mM盐水中(A组),或在10-12期中注入90 mM盐水中(B组) 。 3.在A组中,没有任何剂量的血管紧张素是利尿剂。排尿钠和尿钠浓度是剂量依赖性的。 4.激肽释放酶的排泄量与血管紧张素有关(P <0.0001),与尿钠浓度呈负相关(P = 0.011)。在利钠和非利钠大鼠中,血管紧张素释放后激肽释放酶的排泄与前期尿钠浓度呈负相关。 5.在B组中,利钠和尿钠浓度是剂量依赖性的。在10-13期间,激肽释放酶排泄与前一时期的尿钠浓度呈负相关(P = 0.0001),与在9-13时期的尿渗透压成反比。 6.以5 x 10(-6)微克min-1输注血管紧张素II导致排尿失败。 7.得出了能够分离血管紧张素和尿钠浓度对激肽释放酶排泄的相反作用的配方。在A组中,这两种作用仅在利尿大鼠中有统计学意义(每期利尿> 20摩尔)。在B组中,配方奶粉中激肽释放酶的排泄量呈剂量依赖性增加,而激肽释放酶排泄量的减少与尿钠浓度的增加有关,从而抵消了这种情况。 8.输注0.9%的盐水后,第10至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.在大鼠中的总作用与在狗中的总作用不同,在后者中激肽释放酶随着血管紧张素钠排泄而增加并且尿液发生稀释。

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