Understanding the contribution of Guyton's large circulatory model to long‐term control of arterial pressure

Abstract

With the publication in 1972 of a large computer model of circulatory control, Guyton and colleagues challenged the then prevailing views on how blood pressure and cardiac output were controlled. At that time, it was widely accepted that the heart controlled cardiac output and that peripheral resistance controlled arterial blood pressure. By incorporating the empirically demonstrated concepts of blood flow autoregulation and the pressure–natriuresis relationship into their mathematical model, Guyton and colleagues were able to develop a number of revolutionary concepts. Guyton's circulatory model was particularly instrumental in exploring the linkage between blood pressure and sodium balance and in demonstrating an overriding importance of renal salt and water balance in setting the long‐term blood pressure level. In both the model and experimental data, any long‐lasting imbalance between salt intake and salt excretion leads to a progressive alteration of the degree of filling of the vascular system and thus to parallel changes in blood pressure. In turn, changes in blood pressure alter sodium excretion, opposing the initial salt imbalance. Although Guyton's model does not include the most recent cardiovascular discoveries, the concepts underlying the basic functioning of the cardiovascular system can serve as a well‐built basis for the development of new, large and integrative cardiovascular models.

Pkd1-inactivation in vascular smooth muscle cells and adaptation to hypertension

“…Cardiac output (stroke volume  heart rate) is known to drop upon an increase in blood pressure, as for instance induced by AngII infusion. 34 However, according to the classical Guyton model (Guyton et al, 1972), without autoregulation (ie, myogenic tone), cardiac output in response to hypertension is predicted to remain high. 32,34 This model fits nicely with our data as anticipated by a loss of myogenic tone in SM22-Pkd1 del/del mice.…”

“…34 However, according to the classical Guyton model (Guyton et al, 1972), without autoregulation (ie, myogenic tone), cardiac output in response to hypertension is predicted to remain high. 32,34 This model fits nicely with our data as anticipated by a loss of myogenic tone in SM22-Pkd1 del/del mice. 18 Indeed, in these mice, the decrease in heart rate (ie, cardiac output) is significantly less prominent compared with the control mice.…”

Delaying orthostatic syncope with mental challenge: A pilot study

“…Being a primary capacitance area of the body, the venous system can exert great changes in venous return and cardiac preload when its capacity is altered. In a previous study, in which we studied the effects of mental challenge on orthostatic responses [4], mental challenge-induced sympathetic activity increased cardiac output, being sustained perhaps by a greater increase in venous tone, increased mean circulatory filling pressure and thus increased venous return (see Guyton's analysis [20]). Our results are supported by observations of Kuipers et al that mental challenge induces splanchnic vasoconstriction [3].…”

Integrative physiology in Modelica

“…C. Guyton, Hall, and Montani 1988;J. P. Montani, Mizelle, et al 1989; J. P. ; J.-P. Montani and Van Vliet 2009) or the old model of Ikeda (Ikeda et al 1979). For example, this path was taken by the international research team of the SAPHIR (System Approach for Physiological Integration of Renal, cardiac and respiratory control) project in 2008 after deciding that Figure 5.…”