血管紧张素II长期输注导致的动脉压与血浆血管紧张素II浓度关系的改变。

B L Bean, J J Brown, J Casals-Stenzel, R Fraser, A F Lever, J J Morton, B Petch, A J Riegger, J I Robertson, M Tree
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引用次数: 4

摘要

1. 血管紧张素II以恒定剂量输注狗2周,引起动脉压进行性升高。2. 停药后48 h内血压从高血压水平缓慢下降。每周一次的剂量反应研究显示血浆血管紧张素ii -血压曲线渐进式升高,但没有变陡。4. 因此,在长时间给药血管紧张素II期间,给定的肽血浆浓度可以维持比急性输注时更高的动脉压。
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An altered relation between arterial pressure and plasma angiotensin II concentration resulting from prolonged infusion of angiotensin II.

1. Infusion of angiotensin II into dogs at constant dose over 2 weeks caused a progressive rise in arterial pressure. 2. When the infusion was stopped the pressure dropped slowly from hypertensive levels over 48 h. 3. Dose-response studies at weekly intervals showed progressive elevation, without steepening, of the plasma angiotensin II-blood pressure curve. 4. Thus, during prolonged administration of angiotensin II, a given plasma concentration of the peptide can sustain a higher arterial pressure than it can during acute infusions.

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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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