Guyton Model: Atrial Natriuretic Peptide
Catherine
Lloyd
Auckland Bioengineering Institute, University of Auckland
Model Status
This CellML model has been validated. Due to the differences between procedural code (in this case C-code)
and declarative languages (CellML), some aspects of the original model were not able to be encapsulated by
the CellML model (such as the damping of variables). This may effect the transient behaviour of the model,
however the steady-state behaviour would remain the same. The equations in this file and the steady-state
output from the model conform to the results from the MODSIM program.
Model Structure
Arthur Guyton (1919-2003) was an American physiologist who became famous for his 1950s experiments in which he studied
the physiology of cardiac output and its relationship with the peripheral circulation. The results of these experiments
challenged the conventional wisdom that it was the heart itself that controlled cardiac output. Instead Guyton demonstrated
that it was the need of the body tissues for oxygen which was the real regulator of cardiac output. The "Guyton Curves"
describe the relationship between right atrial pressures and cardiac output, and they form a foundation for understanding
the physiology of circulation.
The Guyton model of fluid, electrolyte, and circulatory regulation is an extensive mathematical model of human circulatory
physiology, capable of simulating a variety of experimental conditions, and contains a number of linked subsystems relating
to circulation and its neuroendocrine control.
This is a CellML translation of the Guyton model of the regulation of the circulatory system. The complete model consists
of separate modules each of which characterise a separate physiological subsystems. The Circulation Dynamics is the primary
system, to which other modules/blocks are connected. The other modules characterise the dynamics of the kidney, electrolytes
and cell water, thirst and drinking, hormone regulation, autonomic regulation, cardiovascular system etc, and these feedback
on the central circulation model. The CellML code in these modules is based on the C code from the programme C-MODSIM created
by Dr Jean-Pierre Montani.
This particular CellML model describes the control of atrial natriuretic peptide secretion by the left and right atria of
the heart. It also calculates a multiplier factor for controlling the resistance of the afferent arterioles (AAR) of the kidneys.
model diagram
A systems analysis diagram for the full Guyton model describing circulation regulation.
model diagram
A schematic diagram of the components and processes described in the current CellML model.
There are several publications referring to the Guyton model. One of these papers is cited below:
Circulation: Overall Regulation, A.C. Guyton, T.G. Coleman, and H.J. Granger, 1972,
Annual Review of Physiology
, 34, 13-44. PubMed ID: 4334846
Terkildsen
Jonna
j.terkildsen@auckland.ac.nz
The University of Auckland
The Bioengineering Institute
2008-04-03
The University of Auckland, Bioengineering Institute
Guyton
Atrial Natriuretic Peptide
Description of Guyton atrial natriuretic peptide module
2008-00-00 00:00
keyword
physiology
organ systems
cardiovascular circulation
vatrial natriuretic peptide
Guyton
This section calculates the control of atrial natriuretic peptide secretion by the
left and right atria of the heart. It also calculates a multiplier factor for
controlling the resistance of the afferent arterioles (AAR) of the kidneys.
Encapsulation grouping component containing all the components in the Atrial Natriuretic Peptide Model.
The inputs and outputs of the Atrial Natriuretic Peptide Model must be passed by this component.
ANP1, ANP2, ANP3, ANP3A, and ANP4:
Calculation of the total amount of atrial natriuretic peptide secreted at
any given time. Block ANP1 determines the pressure level at which changes
in left atrial pressure (PLA) will begin to affect atrinatriuretic peptide
secretion. Block 1A sets a lower limit of zero for this secretion.
Block ANP2 calculates from the pressure level in the right atrium (PRA) the
stimulation of ANP output by the right atrium. Block 3 multiplies the
output of the right atrium by two-fold (against a one-fold amount secreted
by the left atrium). Block 3A sets a lower limit of zero for right atrial
output. Block 4 adds the outputs from the left atrium and right atrium.
ANP5:
Block 5 normalizes the ANP secretion under normal conditions to a value of 1.
ANP1, ANP2, ANP3 and ANP3A:
Calculation of the total amount of atrial natriuretic peptide secreted at
any given time. Block ANP1 determines the pressure level at which changes
in left atrial pressure (PLA) will begin to affect atrinatriuretic peptide
secretion. Block 1A sets a lower limit of zero for this secretion.
Block ANP2 calculates from the pressure level in the right atrium (PRA) the
stimulation of ANP output by the right atrium. Block 3 multiplies the
output of the right atrium by two-fold (against a one-fold amount secreted
by the left atrium). Block 3A sets a lower limit of zero for right atrial
output.
ANP1, ANP2, ANP3 and ANP3A:
Calculation of the total amount of atrial natriuretic peptide secreted at
any given time. Block ANP1 determines the pressure level at which changes
in left atrial pressure (PLA) will begin to affect atrinatriuretic peptide
secretion. Block 1A sets a lower limit of zero for this secretion.
Block ANP2 calculates from the pressure level in the right atrium (PRA) the
stimulation of ANP output by the right atrium. Block 3 multiplies the
output of the right atrium by two-fold (against a one-fold amount secreted
by the left atrium). Block 3A sets a lower limit of zero for right atrial
output.
ANP4 and ANP5:
Block 4 adds the outputs from the left atrium and right atrium. Block 5 normalizes
the ANP secretion under normal conditions to a value of 1.
$\mathrm{ANPL}=\begin{cases}0 & \text{if $(\mathrm{PLA}-1)\times 1< 0$}\\ (\mathrm{PLA}-1)\times 1 & \text{otherwise}\end{cases}\mathrm{ANPR2}=\begin{cases}0 & \text{if $(\mathrm{PRA}+1)\times 2< 0$}\\ (\mathrm{PRA}+1)\times 2 & \text{otherwise}\end{cases}\mathrm{ANP}=\frac{\mathrm{ANPL}+\mathrm{ANPR2}}{3}$
ANP 7:
This block allows infusion of ANP into the circulation (ANPINF). The output
of the block is ANP1 which is the total rate of ANP entering the circulation
at any given time.
ANP 7:
This block allows infusion of ANP into the circulation (ANPINF). The output
of the block is ANP1 which is the total rate of ANP entering the circulation
at any given time.
$\mathrm{ANP1}=\begin{cases}\mathrm{ANPKNS} & \text{if $\mathrm{ANPKNS}> 0$}\\ \mathrm{ANP}+\mathrm{ANPINF} & \text{otherwise}\end{cases}$
ANP8, ANP9, and ANP10:
Calculation of the concentration of ANP in the plasma (ANPC) from the rate of
entry of ANP into the plasma (ANP1). The time constant for build-up of ANP in
the circulation is determined by ANPTC in Block 9. ANPC is normalized to 1.
ANP8, ANP9, and ANP10:
Calculation of the concentration of ANP in the plasma (ANPC) from the rate of
entry of ANP into the plasma (ANP1). The time constant for build-up of ANP in
the circulation is determined by ANPTC in Block 9. ANPC is normalized to 1.
$\frac{d \mathrm{ANPC}}{d \mathrm{time}}=\frac{\mathrm{ANP1}-\mathrm{ANPC}}{\mathrm{ANPTC}}$
ANP11:
This curve calculates a multiplier factor (ANPX) for determining the effect
of ANP on the afferent arteriolar resistance of the kidneys. The upper limit
of ANPX is ANPXUL.
ANP 12:
This block sets the lower limit of ANPX equal to -1.
ANP11:
This curve calculates a multiplier factor (ANPX) for determining the effect
of ANP on the afferent arteriolar resistance of the kidneys. The upper limit
of ANPX is ANPXUL.
ANP 12:
This block sets the lower limit of ANPX equal to -1.
$\mathrm{ANPX1}=\mathrm{ANPXUL}-\frac{\mathrm{ANPXUL}}{0.5555556(1+\mathrm{ANPC})}\mathrm{ANPX}=\begin{cases}-1 & \text{if $\mathrm{ANPX1}< -1$}\\ \mathrm{ANPX1} & \text{otherwise}\end{cases}$