University of Minnesota, Department of Mathematics, Minneapolis, MN, USA.
J Physiol. 2012 Dec 1;590(23):5975-92. doi: 10.1113/jphysiol.2012.228619. Epub 2012 Aug 13.
A conceptually novel mathematical model of neurogenic angiotensin II-salt hypertension is developed and analysed. The model consists of a lumped parameter circulatory model with two parallel vascular beds; two distinct control mechanisms for both natriuresis and arterial resistances can be implemented, resulting in four versions of the model. In contrast with the classical Guyton-Coleman model (GC model) of hypertension, in the standard version of our new model natriuresis is assumed to be independent of arterial pressure and instead driven solely by sodium intake; arterial resistances are driven by increased sympathetic nervous system activity in response to the elevated plasma angiotensin II and increased salt intake (AngII-salt). We compare the standard version of our new model against a simplified Guyton-Coleman model in which natriuresis is a function of arterial pressure via the pressure-natriuresis mechanism, and arterial resistances are controlled via the whole-body autoregulation mechanism. We show that the simplified GC model and the new model correctly predict haemodynamic and renal excretory responses to induced changes in angiotensin II and sodium inputs. Importantly, the new model reproduces the pressure-natriuresis relationship--the correlation between arterial pressure and sodium excretion--despite the assumption of pressure-independent natriuresis. These results show that our model provides a conceptually new alternative to Guyton's theory without contradicting observed haemodynamic changes or pressure-natriuresis relationships. Furthermore, the new model supports the view that hypertension need not necessarily have a renal aetiology and that long-term arterial pressure could be determined by sympathetic nervous system activity without involving the renal sympathetic nerves.
提出并分析了一个神经源性血管紧张素 II-盐高血压的新概念数学模型。该模型由一个具有两个平行血管床的集中参数循环模型组成；可以实现两种独立的利钠和动脉阻力控制机制，从而产生模型的四个版本。与高血压的经典 Guyton-Coleman 模型（GC 模型）相比，在我们新模型的标准版本中，利钠作用被假设为独立于动脉压，而是仅由钠摄入驱动；动脉阻力由增加的交感神经系统活动驱动，以响应升高的血浆血管紧张素 II 和增加的盐摄入（AngII-salt）。我们将我们新模型的标准版本与一个简化的 Guyton-Coleman 模型进行比较，其中利钠作用通过压力-利钠机制作为动脉压的函数，而动脉阻力通过全身自动调节机制进行控制。我们表明，简化的 GC 模型和新模型正确预测了诱导的血管紧张素 II 和钠输入变化对血液动力学和肾脏排泄反应。重要的是，尽管假设利钠作用独立于压力，但新模型再现了压力-利钠关系-动脉压与钠排泄之间的相关性。这些结果表明，我们的模型提供了一种与 Guyton 理论概念上不同的替代方案，而不会与观察到的血液动力学变化或压力-利钠关系相矛盾。此外，新模型支持这样一种观点，即高血压不一定具有肾脏病因，并且长期动脉压可以由交感神经系统活动决定，而不涉及肾交感神经。
