Renin suppression by saline is blunted in nonmodulating essential hypertension.
Renin suppression by saline is blunted in nonmodulating essential hypertension.
复制标题
在非调节性原发性高血压中，盐水对肾素的抑制作用减弱。
DOI：
10.1161/01.hyp.10.4.404
复制
发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Williams,GH
中科院分区：
文献类型：
--
作者：
Rabinowe,SL;Redgrave,JE;Shoback,DM;Podolsky,S;Hollenberg,NK;Williams,GH
我们已经报道，50%的肾素正常的原发性高血压患者在补钠后肾素-血管紧张素-醛固酮轴的延迟抑制和急性盐负荷的排泄延迟。在另一项研究中，我们还描述了一组高血压患者(称为非调节剂)，他们有几种异常，包括对盐负荷的升压反应。为了评估这些不同患者组中描述的异常是否真的发生在同一患者身上，我们评估了38名高血压患者对短期生理盐水负荷的肾素-血管紧张素-醛固酮轴的反应。他们的调节能力是由他们的肾血管对高盐饮食(200mEq Na)中注入的血管紧张素II的反应决定的。在以75mEq/小时的速度输注生理盐水3小时后，正常调制的患者在60分钟和120分钟血浆肾素活性的降低明显大于非调制的患者(p<0.008)。在完全调制的患者中，血浆醛固酮水平也显著降低(p<0.001)。因此，非调节性高血压患者在几个影响钠稳态的系统中存在异常，包括肾上腺和肾脏血管对血管紧张素II的反应改变，肾血流对盐负荷的反应改变，以及短期生理盐水输注对肾素-血管紧张素-醛固酮系统的延迟抑制。
We have reported that 50% of subjects with normal renin essential hypertension have both delayed suppression of the renin-angiotensin-aldosterone axis following sodium infusion and a delayed rate of excretion of an acute salt load. In another study we have also described a subset of patients with essential hypertension (called nonmodulators) who have several abnormalities, including a pressor response to salt loading. To evaluate whether the abnormalities described in these different groups of patients actually occur in the same patient, we assessed the renin-angiotensin-aldosterone axis response to short-term saline loading in 38 hypertensive patients. Their ability to modulate was determined by their renal vascular response to infused angiotensin II on a high salt diet (200 mEq Na). In response to a 3-hour infusion of saline, 75 mEq/hr, the reduction in plasma renin activity at both 60 and 120 minutes was significantly greater (p less than 0.008) in patients with normal modulation than in the nonmodulators. Plasma aldosterone levels were also significantly lower (p less than 0.001) in those with intact modulation. Thus, nonmodulating essential hypertensive patients have abnormalities in several systems that influence sodium homeostasis, including altered adrenal and renal vascular response to angiotensin II, altered renal blood flow response to salt loading, and a delayed suppression of the renin-angiotensin-aldosterone system with short-term saline infusion.