Creatine Kinase in Energy Metabolic Signalling in Muscle
Catherine
Lloyd
Auckland Bioengineering Institute, The University of Auckland
Model Status
This CellML model has been checked in both OpenCell and COR. However the model contains partial differential equations which are currently beyond the scope of the CellML API.
Model Structure
ABSTRACT: The purpose of this study is to investigate theoretically which intracellular factors may be important for regulation of mitochondrial respiration in working heart cells in vivo. We have developed a model that describes quantitatively the published experimental data on dependence of the rate of oxygen consumption and metabolic state of working isolated perfused rat heart on workload over its physiological range (Williamson JR, Ford G, Illingworth J, Safer B. Circ Res 38, Suppl I, I39-I51, 1976). Analysis of this model shows that for phosphocreatine, creatine, and ATP the equilibrium assumption is an acceptable approximation with respect to their diffusion in the intracellular bulk water phase. However, the ADP concentration changes in the contraction cycle in a nonequilibrium workload-dependent manner, showing the existence of the intracellular concentration gradients. The model shows that workload-dependent alteration of ADP concentration in the compartmentalized creatine kinase system may be taken, together with the changes in P(i) concentration, to be among the major components of the metabolic feedback signal for regulation of respiration in muscle cells.
The original paper reference is cited below:
Regulation of mitochondrial respiration in heart cells analyzed by reaction-diffusion model of energy transfer, Marko Vendelin, Olav Kongas, and Valdur Saks, 2000, American Journal of Physiology - Cell Physiology, 278, C747-C764. PubMed ID: 10751324
Schematic diagram of the two-dimensional compartmentalised energy transfer model of cardiac cells: the components of the model. The total diffusion pathway is 1.2 micrometres, including the outer mitochondrial membrane, the layer of myoplasm and the myofibril. Creatine kinase (CK) and myosin magnesium ATPase activities are distributed non-uniformly along the myofibril.
ATP
adenosine triphosphate
ADP
adenosine diphosphate
AMP
adenosine monophosphate
PCr
phosphocreatine
Cr
creatine
Pi
inorganic phosphate
fATP
total Mg-free adenosine triphosphate
fATPx
mitochondrial matrix Mg-free adenosine triphosphate
fATPext
Cytoplasmic Mg-free adenosine triphosphate
fATPg
microcompartment Mg-free adenosine triphosphate
fATPi
mitochondrial IM space Mg-free adenosine triphosphate
mATP
total Mg-bound adenosine triphosphate
mATPx
mitochondrial matrix Mg-bound adenosine triphosphate
mATPext
myoplasmic Mg-bound adenosine triphosphate
mATPg
microcompartment Mg-bound adenosine triphosphate
mATPi
mitochondrial IM space Mg-bound adenosine triphosphate
fADP
total Mg-free adenosine diphosphate
fADPx
mitochondrial matrix Mg-free adenosine diphosphate
fADPext
myoplasmic Mg-free adenosine diphosphate
fADPg
microspace Mg-free adenosine diphosphate
fADPi
mitochondrial IM space Mg-free adenosine diphosphate
mADP
total Mg-bound adenosine diphosphate
mADPx
mitochondrial matrix Mg-bound adenosine diphosphate
mADPext
myoplasmic Mg-bound adenosine diphosphate
mADPg
microspace Mg-bound adenosine diphosphate
mADPi
mitochondrial IM space Mg-bound adenosine diphosphate
H_ATP
ATP hydrolysis function
G_CK
spatial distribution of CK
G_AK
spatial distribution of AK
G_H
spatial distribution of ATPase
ATPi
IM space adenosine triphosphate
ADPi
IM space adenosine diphosphate
AMPi
IM space adenosine monophosphate
PCri
IM space phosphocreatine
Cri
IM space creatine
Pii
IM space creatine
UQ
oxidised coenzyme Q
c3plus
oxidised cytochrome c
NAD
matrix NAD
Hx
matrix H
ATPx
matrix ATP
Pix
matrix Pi
The University of Auckland
Auckland Bioengineering Institute
Marko
Vendelin
Catherine
Lloyd
May
This file contains a CellML description of Vendelin et al.'s mathematical model of mitochondrial respiration in heart cells.
c.lloyd@auckland.ac.nz
Catherine Lloyd
Regulation of mitochondrial respiration in heart cells analyzed by reaction-diffusion model of energy transfer
278
C747
C764
Olav
Kongas
2003-11-06T00:00:00+13:00
2000-00-00 00:00
keyword
electrophysiology
cardiac
mitochondria
Valdur
Saks
Catherine Lloyd
10751324
American Journal of Physiology Cell Physiology
This CellML model has been checked in both PCEnv and COR. However the model contains partial differential equations which are currently beyond the scope of the tools.