Implementation of a Model of Bodily Fluids Regulation

Abstract

The classic model of blood pressure regulation by Guyton et al. (Annu Rev Physiol 34:13–46, 1972a; Ann Biomed Eng 1:254–281, 1972b) set a new standard for quantitative exploration of physiological function and led to important new insights, some of which still remain the focus of debate, such as whether the kidney plays the primary role in the genesis of hypertension (Montani et al. in Exp Physiol 24:41–54, 2009a; Exp Physiol 94:382–388, 2009b; Osborn et al. in Exp Physiol 94:389–396, 2009a; Exp Physiol 94:388–389, 2009b). Key to the success of this model was the fact that the authors made the computer code (in FORTRAN) freely available and eventually provided a convivial user interface for exploration of model behavior on early microcomputers (Montani et al. in Int J Bio-med Comput 24:41–54, 1989). Ikeda et al. (Ann Biomed Eng 7:135–166, 1979) developed an offshoot of the Guyton model targeting especially the regulation of body fluids and acid–base balance; their model provides extended renal and respiratory functions and would be a good basis for further extensions. In the interest of providing a simple, useable version of Ikeda et al.’s model and to facilitate further such extensions, we present a practical implementation of the model of Ikeda et al. (Ann Biomed Eng 7:135–166, 1979), using the ODE solver Berkeley Madonna.Electronic supplementary materialThe online version of this article (doi:10.1007/s10441-015-9250-3) contains supplementary material, which is available to authorized users.

Extracellular Fluid Excess Is Significantly Associated With Coronary Artery Calcification in Patients With Chronic Kidney Disease

“…In the presence of ECF excess, urinary excretion of sodium and fluid is increased through a negative feedback mechanism to maintain fluid homeostasis. However, if renal function is impaired, urinary excretion of sodium and fluid is reduced and the intrarenal renin–angiotensin–aldosterone system is triggered, leading to persistent and exacerbated ECF excess 26, 27. This persistent ECF excess results in pathologic mechanical stimuli on vascular endothelial and smooth muscle cells (VSMCs).…”

Association of Extracellular Fluid Excess with Choroidal Vascular Index in Patients with Chronic Kidney Disease.

“…Angiotensin II acts as a powerful vasoconstrictor, and promotes sympathetic overactivity through the regulation of central sympathetic outflow. [19,20] This interaction could potentially contribute to the decrease in the CVI. Furthermore, the persistent ECF excess results in pathological mechanical stimuli on vascular endothelial and smooth muscle cells.…”

Dynamic analysis of the individual patterns of intakes, voids, and bladder sensations reported in bladder diaries collected in the LURN study

“…BDs. There are several mathematical models analyzing renal physiology and urine production, including neural control of kidney function [9][10][11][12][13][14][15][16]. These models provide helpful insights for understanding physiology of urination; however, they do not allow for the prediction of adverse urinary events or identification of behavioral modifications to avoid such events.…”