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MODEL0491251823 - Chen2007_NeuronalEndothelialNOS

 

The following model is part of the non-curated branch of BioModels Database. While the syntax of the model has been verified, its semantics remains unchecked. Any annotation present in the models is not a product of BioModels' annotators. We are doing our best to incorporate this model into the curated branch as soon as possible. In the meantime, we display only limited metadata here. For further information about the model, please download the SBML file.


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Reference Publication
Publication ID: 17320763
Chen K, Popel AS.
Vascular and perivascular nitric oxide release and transport: biochemical pathways of neuronal nitric oxide synthase (NOS1) and endothelial nitric oxide synthase (NOS3).
Free Radic. Biol. Med. 2007 Mar; 42(6): 811-822
Department of Biomedical Engineering, 613 Traylor Building, 720 Rutland Avenue, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA. kchen21@jhu.edu  [more]
Model
Original Model: CellML logo
Submitter: Vijayalakshmi Chelliah
Submission Date: 24 Apr 2009 13:55:13 UTC
Last Modification Date: 24 Apr 2009 13:55:13 UTC
Creation Date: 24 Apr 2009 13:55:13 UTC
Encoders:
bqbiol:occursIn Brenda Tissue Ontology arteriole
bqbiol:hasTaxon Taxonomy Homo sapiens
bqbiol:isVersionOf Gene Ontology regulation of nitric-oxide synthase activity
bqmodel:isDerivedFrom PubMed 16864000
Notes

This a model from the article:
Vascular and perivascular nitric oxide release and transport: biochemical pathways of neuronal nitric oxide synthase (NOS1) and endothelial nitric oxide synthase (NOS3).
Chen K, Popel AS Free Radic Biol Med. 2007 Mar 15;42(6):811-22. 17320763 ,
Abstract:
Nitric oxide (NO) derived from nitric oxide synthase (NOS) is an important paracrine effector that maintains vascular tone. The release of NO mediated by NOS isozymes under various O(2) conditions critically determines the NO bioavailability in tissues. Because of experimental difficulties, there has been no direct information on how enzymatic NO production and distribution change around arterioles under various oxygen conditions. In this study, we used computational models based on the analysis of biochemical pathways of enzymatic NO synthesis and the availability of NOS isozymes to quantify the NO production by neuronal NOS (NOS1) and endothelial NOS (NOS3). We compared the catalytic activities of NOS1 and NOS3 and their sensitivities to the concentration of substrate O(2). Based on the NO release rates predicted from kinetic models, the geometric distribution of NO sources, and mass balance analysis, we predicted the NO concentration profiles around an arteriole under various O(2) conditions. The results indicated that NOS1-catalyzed NO production was significantly more sensitive to ambient O(2) concentration than that catalyzed by NOS3. Also, the high sensitivity of NOS1 catalytic activity to O(2) was associated with significantly reduced NO production and therefore NO concentrations, upon hypoxia. Moreover, the major source determining the distribution of NO was NOS1, which was abundantly expressed in the nerve fibers and mast cells close to arterioles, rather than NOS3, which was expressed in the endothelium. Finally, the perivascular NO concentration predicted by the models under conditions of normoxia was paradoxically at least an order of magnitude lower than a number of experimental measurements, suggesting a higher abundance of NOS1 or NOS3 and/or the existence of other enzymatic or nonenzymatic sources of NO in the microvasculature.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Chen K, Popel AS (2007) - version02
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute

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