Dataset Information

Sarai2003_CardiacSAnodePacemaker

ABSTRACT: This a model from the article: Role of individual ionic current systems in the SA node hypothesized by a model study. Sarai N, Matsuoka S, Kuratomi S, Ono K, Noma A. Jpn J Physiol 2003 Apr;53(2):125-34 12877768 , Abstract: This paper discusses the development of a cardiac sinoatrial (SA) node pacemaker model. The model successfully reconstructs the experimental action potentials at various concentrations of external Ca2+ and K+. Increasing the amplitude of L-type Ca2+ current (I(CaL)) prolongs the duration of the action potential and thereby slightly decreases the spontaneous rate. On the other hand, a negative voltage shift of I(CaL) gating by a few mV markedly increases the spontaneous rate. When the amplitude of sustained inward current (I(st)) is increased, the spontaneous rate is increased irrespective of the I(CaL) amplitude. Increasing [Ca2+](o) shortens the action potential and increases the spontaneous rate. When the spontaneous activity is stopped by decreasing I(CaL) amplitude, the resting potential is nearly constant (-35 mV) over 1-15 mM [K+](o) as observed in the experiment. This is because the conductance of the inward background non-selective cation current balances with the outward [K+](o)-dependent K+ conductance. The unique role of individual voltage- and time-dependent ion channels is clearly demonstrated and distinguished from that of the background current by calculating an instantaneous zero current potential ("lead potential") during the course of the spontaneous activity. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Sarai N, Matsuoka S, Kuratomi S, Ono K, Noma A. (2003) - version=1.0 The original CellML model was created by: Alan Garny alan.garny@dpag.ox.ac.uk The University of Oxford This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

SUBMITTER: Camille Laibe

PROVIDER: MODEL1006230108 | BioModels | 2005-01-01

REPOSITORIES: BioModels

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Publications

Role of individual ionic current systems in the SA node hypothesized by a model study.

Sarai Nobuaki N Matsuoka Satoshi S Kuratomi Shinobu S Ono Kyoichi K Noma Akinori A

The Japanese journal of physiology 20030401 2

This paper discusses the development of a cardiac sinoatrial (SA) node pacemaker model. The model successfully reconstructs the experimental action potentials at various concentrations of external Ca2+ and K+. Increasing the amplitude of L-type Ca2+ current (I(CaL)) prolongs the duration of the action potential and thereby slightly decreases the spontaneous rate. On the other hand, a negative voltage shift of I(CaL) gating by a few mV markedly increases the spontaneous rate. When the amplitude o ...[more]

PMID: 12877768

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Project description:This a model from the article: Role of individual ionic current systems in ventricular cells hypothesized by a model study. Matsuoka S, Sarai N, Kuratomi S, Ono K, Noma A. Jpn J Physiol 2003 Apr;53(2):105-23 12877767 , Abstract: Individual ion channels or exchangers are described with a common set of equations for both the sinoatrial node pacemaker and ventricular cells. New experimental data are included, such as the new kinetics of the inward rectifier K+ channel, delayed rectifier K+ channel, and sustained inward current. The gating model of Shirokov et al. (J Gen Physiol 102: 1005-1030, 1993) is used for both the fast Na+ and L-type Ca2+ channels. When combined with a contraction model (Negroni and Lascano: J Mol Cell Cardiol 28: 915-929, 1996), the experimental staircase phenomenon of contraction is reconstructed. The modulation of the action potential by varying the external Ca2+ and K+ concentrations is well simulated. The conductance of I(CaL) dominates membrane conductance during the action potential so that an artificial increase of I(to), I(Kr), I(Ks), or I(KATP) magnifies I(CaL) amplitude. Repolarizing current is provided sequentially by I(Ks), I(Kr), and I(K1). Depression of ATP production results in the shortening of action potential through the activation of I(KATP). The ratio of Ca2+ released from SR over Ca2+ entering via I(CaL) (Ca2+ gain = approximately 15) in excitation-contraction coupling well agrees with the experimental data. The model serves as a predictive tool in generating testable hypotheses. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Matsuoka S, Sarai N, Kuratomi S, Ono K, Noma A. (2003) - version=1.0 The original CellML model was created by: Penny Noble penny.noble@dpag.ox.ac.uk The University of Oxford This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not. . To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

Project description:Wang2008 - Mimicking the inhibitory effect of riluzole on membrane conductance in skeletal fibres This model is described in the article: Riluzole-induced block of voltage-gated Na+ current and activation of BKCa channels in cultured differentiated human skeletal muscle cells. Wang YJ, Lin MW, Lin AA, Wu SN. Life Sci. 2008 Jan; 82(1-2): 11-20 Abstract: Riluzole is known to be of therapeutic use in the management of amyotrophic lateral sclerosis. In this study, we investigated the effects of riluzole on ion currents in cultured differentiated human skeletal muscle cells (dHSkMCs). Western blotting revealed the protein expression of alpha-subunits for both large-conductance Ca2+-activated K+ (BK(Ca)) channel and Na+ channel (Na(v)1.5) in these cells. Riluzole could reduce the frequency of spontaneous beating in dHSkMCs. In whole-cell configuration, riluzole suppressed voltage-gated Na+ current (I(Na)) in a concentration-dependent manner with an IC50 value of 2.3 microM. Riluzole (10 microM) also effectively increased Ca2+-activated K+ current (I(K(Ca))) which could be reversed by iberiotoxin (200 nM) and paxilline (1 microM), but not by apamin (200 nM). In inside-out patches, when applied to the inside of the cell membrane, riluzole (10 microM) increased BK(Ca)-channel activity with a decrease in mean closed time. Simulation studies also unraveled that both decreased conductance of I(Na) and increased conductance of I(K(Ca)) utilized to mimic riluzole actions in skeletal muscle cells could combine to decrease the amplitude of action potentials and increase the repolarization of action potentials. Taken together, inhibition of I(Na) and stimulation of BK(Ca)-channel activity caused by this drug are partly, if not entirely, responsible for its muscle relaxant actions in clinical setting. This model is hosted on BioModels Database and identified by: BIOMD0000000693. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Project description:This the model describing the action potentials of the peripheral rabbit sinoatrial node from the article: Mathematical models of action potentials in the periphery and center of the rabbit sinoatrial node. Mathematical models of action potentials in the periphery and center of the rabbit sinoatrial node. Am J Physiol Heart Circ Physiol. 2000 Jul;279(1):H397-421. Pubmed ID: 10899081 , full text at AJP - Heart and Circulatory Physiology. Abstract: Mathematical models of the action potential in the periphery and center of the rabbit sinoatrial (SA) node have been developed on the basis of published experimental data. Simulated action potentials are consistent with those recorded experimentally: the model-generated peripheral action potential has a more negative takeoff potential, faster upstroke, more positive peak value, prominent phase 1 repolarization, greater amplitude, shorter duration, and more negative maximum diastolic potential than the model-generated central action potential. In addition, the model peripheral cell shows faster pacemaking. The models behave qualitatively the same as tissue from the periphery and center of the SA node in response to block of tetrodotoxin-sensitive Na(+) current, L- and T-type Ca(2+) currents, 4-aminopyridine-sensitive transient outward current, rapid and slow delayed rectifying K(+) currents, and hyperpolarization-activated current. A one-dimensional model of a string of SA node tissue, incorporating regional heterogeneity, coupled to a string of atrial tissue has been constructed to simulate the behavior of the intact SA node. In the one-dimensional model, the spontaneous action potential initiated in the center propagates to the periphery at approximately 0.06 m/s and then into the atrial muscle at 0.62 m/s. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Zhang, Holden, Kodama, Honjo, Lei, Varghese, Boyett, 2000, version03 The original CellML model was created and curated by: Garny, Alan alan.garny(at)dpag.ox.ac.uk University of Oxford This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

Project description:Aim; To identify genes which are differentially expressed between calcicoles and non- calcicoles. Background; Grasslands on the calcareous soils of chalk and other limestones are among the most species-rich plant communities in Europe (Rodwell 1991 et seq.). They have experienced huge losses and remain vulnerable to such impacts as neglect of traditional management, agricultural improvement and global changes in climate, nitrogen depositions and ozone levels. Our understanding of the physiological characteristics of calcicoles and calcifuges remains limited. A detailed understanding of the genetic basis of the mechanisms that enable calcicoles to thrive on calcareous soils is essential to enable us to predict how these plant communities and their constituent species will be affected by environmental change and how the biodiversity of these ecosystems can be sustained.At Lancaster we have been studying calcicole-calcifuge physiology, with particular reference to Ca2+-tolerance, for over fifteen years. Recently, our research has focused on the regulation of apoplastic Ca2+ in Arabidospsis thaliana. We have compared the response of two ecotypes of A. thaliana, the non-calcicole ecotype Columbia (Col-4) and the calcicole ecotype Cal-0, which is a genetically uniform line from an original population collected by Ratcliffe from a rocky limestone slope in 1954, to rhizospheric Ca2+. Our results show that Cal-0, exhibits a markedly higher tolerance to growth on high rhizospheric Ca2+ compared to Col-4.Our hypothesis is that adaptation to a calcareous environment will be reflected in altered gene expression. To test this hypothesis we will grow Col-4 and Cal-0 at low (1 mM) and high (12.5 mM) rhizospheric Ca2+ and compare the patterns of gene expression by microarray analysis. In the first instance, to eliminate any differences in gene expression between the Cal-0 and Col-4 ecotypes, we will compare RNA that will be extracted using the Qiagen RNEasy kits, from plants grown at 16 hour day lengths and will be harvested after 30 days of growth on sand watered with 0.5 X Long Ashton solution containing 1 mM CaCl2. Experimenter name = Bev Abram; Experimenter phone = 01524 65201ext93524; Experimenter fax = 01524 843854; Experimenter address = Biological Sciences; Experimenter address = Lancaster University; Experimenter address = Bailrigg; Experimenter address = Lancaster; Experimenter zip/postal_code = LA1 4YQ; Experimenter country = UK Experiment Overall Design: 8 samples were used in this experiment

Project description:This a model from the article: Ionic mechanisms underlying human atrial action potential properties: insights from a mathematical model. Courtemanche M, Ramirez RJ, Nattel S. Am J Physiol 1998 Jul;275(1 Pt 2):H301-21 9688927 , Abstract: The mechanisms underlying many important properties of the human atrial action potential (AP) are poorly understood. Using specific formulations of the K+, Na+, and Ca2+ currents based on data recorded from human atrial myocytes, along with representations of pump, exchange, and background currents, we developed a mathematical model of the AP. The model AP resembles APs recorded from human atrial samples and responds to rate changes, L-type Ca2+ current blockade, Na+/Ca2+ exchanger inhibition, and variations in transient outward current amplitude in a fashion similar to experimental recordings. Rate-dependent adaptation of AP duration, an important determinant of susceptibility to atrial fibrillation, was attributable to incomplete L-type Ca2+ current recovery from inactivation and incomplete delayed rectifier current deactivation at rapid rates. Experimental observations of variable AP morphology could be accounted for by changes in transient outward current density, as suggested experimentally. We conclude that this mathematical model of the human atrial AP reproduces a variety of observed AP behaviors and provides insights into the mechanisms of clinically important AP properties. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Courtemanche M, Ramirez RJ, Nattel S. (1998) - version03 The original CellML model was created by: Noble, Penny, J penny.noble@dpag.ox.ac.uk Oxford University Department of Physiology, Anatomy & Genetics This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

Project description:Aim To identify genes which are differentially expressed between calcicoles and non- calcicoles. Background Grasslands on the calcareous soils of chalk and other limestones are among the most species-rich plant communities in Europe (Rodwell 1991 et seq.). They have experienced huge losses and remain vulnerable to such impacts as neglect of traditional management, agricultural improvement and global changes in climate, nitrogen depositions and ozone levels. Our understanding of the physiological characteristics of calcicoles and calcifuges remains limited. A detailed understanding of the genetic basis of the mechanisms that enable calcicoles to thrive on calcareous soils is essential to enable us to predict how these plant communities and their constituent species will be affected by environmental change and how the biodiversity of these ecosystems can be sustained.At Lancaster we have been studying calcicole-calcifuge physiology, with particular reference to Ca2+-tolerance, for over fifteen years. Recently, our research has focused on the regulation of apoplastic Ca2+ in Arabidospsis thaliana. We have compared the response of two ecotypes of A. thaliana, the non-calcicole ecotype Columbia (Col-4) and the calcicole ecotype Cal-0, which is a genetically uniform line from an original population collected by Ratcliffe from a rocky limestone slope in 1954, to rhizospheric Ca2+. Our results show that Cal-0, exhibits a markedly higher tolerance to growth on high rhizospheric Ca2+ compared to Col-4.Our hypothesis is that adaptation to a calcareous environment will be reflected in altered gene expression. To test this hypothesis we will grow Col-4 and Cal-0 at low (1 mM) and high (12.5 mM) rhizospheric Ca2+ and compare the patterns of gene expression by microarray analysis. In the first instance, to eliminate any differences in gene expression between the Cal-0 and Col-4 ecotypes, we will compare RNA that will be extracted using the Qiagen RNEasy kits, from plants grown at 16 hour day lengths and will be harvested after 30 days of growth on sand watered with 0.5 X Long Ashton solution containing 1 mM CaCl2. Experimenter name = Bev Abram Experimenter phone = 01524 65201ext93524 Experimenter fax = 01524 843854 Experimenter address = Biological Sciences Experimenter address = Lancaster University Experimenter address = Bailrigg Experimenter address = Lancaster Experimenter zip/postal_code = LA1 4YQ Experimenter country = UK Keywords: strain_or_line_design

Dataset Information

Sarai2003_CardiacSAnodePacemaker

Publications

Role of individual ionic current systems in the SA node hypothesized by a model study.

Similar Datasets

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