人体内有活性和无活性肾素的不同分泌模式。

A M Kappelgaard, J Giese, H Ibsen, M D Nielsen, A Rabøl
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引用次数: 34

摘要

1. 在正常受试者和未经治疗的原发性高血压患者的血浆样本中,无活性肾素浓度(酸化后测量)平均比活性肾素浓度(未酸化时测量)高4-5倍。血浆血管紧张素II浓度与活性肾素相关,与失活肾素无关。3.输注萨拉拉西素引起的超急性刺激导致活性肾素显著升高,而非活性肾素保持不变。4. 由氟塞胺和运动引起的急性刺激导致活性肾素的显著升高和非活性肾素的轻微但显著升高。5. 口服噻嗪超过5天的刺激诱导活性肾素增加7倍,非活性肾素增加一倍。噻嗪治疗3个月导致活性肾素上升4倍,非活性肾素上升3倍。6. 12例肾血管性高血压患者全身血浆、同侧和对侧肾静脉血浆中失活肾素的浓度在输注萨拉拉西辛前后均无差异,且血压下降无相关性。7. 我们的结论是,与人体分泌或释放活性和非活性肾素有关的时间常数是不同的数量级。
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Different secretion patterns of active and inactive renin in man.

1. In plasma samples from normal subjects and patients with untreated essential hypertension, the concentration of inactive renin (as measured after acidification) was on average 4-5 times higher than the concentration of active renin (as measured without acidification).2. Plasma angiotensin II concentration was correlated to active renin but not to inactive renin. 3. A hyperacute stimulation induced by infusion of saralasin resulted in a marked rise of active renin, whereas inactive renin remained unchanged. 4. An acute stimulation induced by frusemide and ambulation led to a considerable rise in active renin and a slight, but significant, rise of inactive renin. 5. Stimulation with oral thiazide over 5 days induced a seven-fold rise of active renin, with a doubling of inactive renin. Thiazide treatment for 3 months led to a four-fold rise of active renin and a three-fold rise of inactive renin. 6. There was no difference between the concentrations of inactive renin in systemic plasma, ipsilateral and contralateral renal venous plasma in 12 patients with renovascular hypertension, neither before nor after infusion of saralasin with the associated fall in blood pressure. 7. We conclude that the time constants pertinent to secretion or release of active and inactive renin in man are of different orders of magnitude.

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Proceedings of the Fifth Meeting of the International Society of Hypertension, Paris, 12-14 June 1978. Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. Definitive evidence for renin in rat brain by affinity chromatographic separation from protease. Renal release of active and inactive renin in essential and renovascular hypertension.
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