Activation of the Renin‐Angiotensin System by Sodium Nitroprusside in Essential Hypertension
Activation of the Renin‐Angiotensin System by Sodium Nitroprusside in Essential Hypertension
复制标题
硝普钠在原发性高血压中激活肾素-血管紧张素系统
DOI：
10.1097/00005344-198401000-00029
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发表时间：
1984
影响因子：
3
通讯作者：
T. Keeton
中科院分区：
文献类型：
--
作者：
A. Shepherd;W. Pinkley;M. Lin;J. McNay;T. Keeton
我们以前已经证明，交感神经系统的激活程度与高血压患者引起的血管抑制程度成正比。在本研究中，研究了肾素-血管紧张素系统在调节硝普钠的血管降压反应中的作用。9例接受利尿剂治疗的住院高血压患者连续给予硝普钠递增剂量，剂量范围为0.0 5~4.8μg/kg/min，每次10min。测定各剂量硝普钠治疗前后的平均动脉压(MAP)、心率(HR)、血浆肾素活性(PRA)和去甲肾上腺素(NE)浓度。随着硝普钠剂量的增加，每个患者的PRA呈逐步增加的趋势。PRA升高与血浆NE浓度升高和MAP降低成正比。然而，在这些关系中发现了相当大的受试者间差异。经多元线性逐步回归分析，血管抑制程度与基线血压和压力感受器反射敏感性有关(r=0.97)。然而，PRA的增加并不是血管降压反应的独立决定因素。因此，肾素血管紧张素系统可能不是这些患者对血管抑制的急性稳态反应的重要组成部分。
We previously have demonstrated that the sympathetic nervous system is activated proportionately to the degree of vasodepression induced in hypertensive patients. In the present study, the role of the renin-angiotensin system in modulating the vasodepressor response to sodium nitroprusside was examined. Nine hospitalized hypertensive patients receiving a diuretic were given serially incremental doses of sodium nitroprusside over a dose range of 0.05–4.8 μg/kg/min with each dose being infused for 10 min. Mean arterial pressure (MAP), heart rate (HR), plasma renin activity (PRA), and plasma norepinephrine (NE) concentration were measured prior to and during each dose level of sodium nitroprusside. Step-wise increments in PRA were seen in each patient as the dose of sodium nitroprusside was increased. The increase in PRA was proportional to the increase in plasma NE concentration and to the decrease in MAP in each patient. However, considerable intersubject variation was seen in these relationships. When examined by multiple linear stepwise regression analysis, the degree of vasodepression was found to be dependent on the baseline blood pressure and baroreflex sensitivity (r = 0.97). However, increment in PRA was not an independent determinant of the vasodepressor response. Thus, the renin angiotensin system may not be a significant component of the acute homeostatic response to vasodepression in these patients.