Millar J A
Clin Exp Hypertens A. 1982;4(11-12):2415-24. doi: 10.3109/10641968209062399.
Release of active renin is inhibited by angiotensin II. To determine whether plasma inactive renin is also sensitive to this hormone, the effect of stepwise infusion of angiotensin II at 5,10 and 20 ng/kg/min on active and inactive renin levels was measured in six salt-replete normal subjects. Each subject received two infusions of angiotensin II on each of 2 study days. The calcium antagonist drug nifedipine (20 mg) or placebo was administered between the angiotensin infusions on each study day. During control infusions there was a significant decline in plasma active renin but no change in inactive renin was observed. Active renin concentration was increased after nifedipine treatment and suppressed to a similar degree by angiotensin II as in control infusions, with no corresponding changes in inactive renin. These studies suggest that plasma inactive renin levels are not subject to feedback inhibition by angiotensin II, and that inactive renin is not a physiologically important precursor of active renin in man.
活性肾素的释放受到血管紧张素II的抑制。为了确定血浆中的无活性肾素是否也对这种激素敏感，在6名盐充足的正常受试者中，测量了以5、10和20 ng/kg/分钟的剂量逐步输注血管紧张素II对活性和无活性肾素水平的影响。在2个研究日中的每一天，每位受试者接受两次血管紧张素II输注。在每个研究日的血管紧张素输注之间给予钙拮抗剂药物硝苯地平（20 mg）或安慰剂。在对照输注期间，血浆活性肾素显著下降，但未观察到无活性肾素的变化。硝苯地平治疗后活性肾素浓度升高，血管紧张素II将其抑制到与对照输注相似的程度，而无活性肾素没有相应变化。这些研究表明，血浆无活性肾素水平不受血管紧张素II的反馈抑制，并且无活性肾素在人体内不是活性肾素的重要生理前体。
