Pharmacological modulation of the renin-angiotensin system by mathematical modeling.

N Pérez-Rosas, J Rodríguez-González
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Abstract

The renin-angiotensin system (RAS) is one of the most important systems in blood pressure homeostasis and pathogenesis of cardiovascular-renal diseases. When blood volume goes down, juxtaglomerular cells in the kidneys secrete renin. Renin stimulates the production of angiotensin I (Ang I), which is then converted to angiotensin II (Ang II). Angiotensin II causes blood vessels to constrict, resulting in increased blood pressure. If the renin angiotensin system is over active, blood pressure will be too high. Most hypotensive drugs are designed to block this system at different points in the pathway. In this study, we developed a mathematical model of the renin-angiotensin system to emulate the response of the renin-angiotensin system in humans. This model consists of a set of differential equations. Special attention is paid to the estimation of all the model parameters from reported experimental data. These equations allow us to model hypertensive and normotensive patients and pharmacotherapeutic approaches to treatment. We show dose-response curves of blood pressure and biochemical components of the renin-angiotensin system. Our results reproduce clinical outcomes. We conclude that mathematical modeling of RAS is a useful approach for gaining insight into the complexities of homeostatic control of arterial pressure and pharmacotherapeutics.

肾素-血管紧张素系统的数学模型药理调节。
肾素-血管紧张素系统(RAS)是血压稳态和心血管-肾脏疾病发病机制中最重要的系统之一。当血容量下降时,肾脏肾小球旁细胞分泌肾素。肾素刺激血管紧张素I (Ang I)的产生,然后转化为血管紧张素II (Ang II),血管紧张素II导致血管收缩,导致血压升高。如果肾素血管紧张素系统过度活跃,血压就会过高。大多数降压药物被设计成在通路的不同点阻断该系统。在这项研究中,我们开发了一个肾素-血管紧张素系统的数学模型来模拟人类肾素-血管紧张素系统的反应。这个模型由一组微分方程组成。特别注意的是所有模型参数的估计从报告的实验数据。这些方程使我们能够对高血压和正常血压患者以及药物治疗方法进行建模。我们展示了血压和肾素-血管紧张素系统生化成分的剂量-反应曲线。我们的结果再现了临床结果。我们得出的结论是,RAS的数学建模是一种有用的方法,可以深入了解动脉压力和药物治疗的稳态控制的复杂性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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