Model Status
This model is known to run in both OpenCell and COR to reproduce the output shown in the publication.
Model Structure
ABSTRACT: We developed a model of the rat ventricular myocyte at room temperature to predict the relative effects of different mechanisms on the cause of the slow increase in force in response to a step change in muscle length. We performed simulations in the presence of stretch-dependent increases in flux through the Na+-H+ exchanger (NHE) and chloride-bicarbonate exchanger (AE), stretch-activated channels (SAC), and the stretch-dependent nitric oxide (NO) induced increased open probability of the ryanodine receptors to estimate the capacity of each mechanism to produce the slow force response (SFR). Inclusion of stretch-dependent NHE & AE, SACs, and stretch-dependent NO effects caused an increase in tension following 15 min of stretch of 0.87%, 32%, and 0%, respectively. Comparing [Ca2+]i dynamics before and after stretch in the presence of combinations of the three stretch-dependent elements, which produced significant SFR values (>20%), showed that the inclusion of stretch-dependent NO effects produced [Ca2+]i transients, which were not consistent with experimental results. Further simulations showed that in the presence of SACs and the absence of stretch-dependent NHE & AE inhibition of NHE attenuated the SFR, such that reduced SFR in the presence of NHE blockers does not indicate a stretch dependence of NHE. Rather, a functioning NHE is responsible for a portion of the SFR. Based on our simulations we estimate that in rat cardiac myocytes at room temperature SACs play a significant role in producing the SFR, potentially in the presence of stretch-dependent NHE & AE and that NO effects, if any, must involve more mechanisms than just increasing the open probability of ryanodine receptors.
The complete original publication reference is cited below:
A mathematical model of the slow force response to stretch in rat ventricular myocytes, Steven Niederer, Nicholas Smith, 2007.
Biophysical Journal, 92 (11) 4030-4044, PubMed ID: 17369410
reaction diagram
Schematic representation of the mathematical model.
keyword
electrophysiology
cardiac
The University of Auckland
17369410
Nicholas
Smith
P
Biophysical Journal
James Lawson
A Mathematical Model of the Slow Force Response to Stretch in Rat Ventricular Myocytes
92
4030
4044
This cell model provides a descripition of the Electrophysiology, Calcium, pH and Mechanics of the rat ventricular myocte at room temperature.
The model includes representations of length dependent channels NHE & AE and RyR, that can be turned on or off as desired. The model was used to demonstrate the importance of stretch activated channels in regulating the slow force response.
It has also been used in tissue models and can be readily coupled to tissue deformation models (Niederer and Smith Progress in Biophysics and Molecular Biology 2007).
The model uses Hinch 2004 (Biophysical Journal) Ca++ dynamics, Pandit 2001 rat electrophysiology and Niederer 2006 mechanics.
2007-06-01 00:00
Steven Niederer
Steven
Niederer
This CellML model has been created by the author of the paper on which it is based. It has been curated to a high standard and is known to reproduce the published results in PCEnv and COR.
10000
10000
Steven
Niederer
A
2008-02-02T00:00:00+13:00
The University of Auckland
Auckland Bioengineering Institute
s.niederer@gmail.com