Izvestiya of Saratov University.

Physics

ISSN 1817-3020 (Print)
ISSN 2542-193X (Online)


For citation:

Neganova A. I., Postnov D. E. Mathematical Modeling of Endothelium-Induced Smooth Muscle Cell Relaxation. Izvestiya of Saratov University. Physics , 2012, vol. 12, iss. 1, pp. 37-42. DOI: 10.18500/1817-3020-2012-12-1-37-42

This is an open access article distributed under the terms of Creative Commons Attribution 4.0 International License (CC-BY 4.0).
Full text:
(downloads: 164)
Language: 
Russian
Heading: 
UDC: 
577.31

Mathematical Modeling of Endothelium-Induced Smooth Muscle Cell Relaxation

Autors: 
Neganova Anastasia Iur'evna, Saratov State University
Postnov Dmitry Engelevich, Saratov State University
Abstract: 

By means of computer modeling we investigate the characteristics of the local mechanisms of regulation of contractile activity of smooth muscle cells. Influence of the endothelium is modeled as the increase of nitric oxide (NO) concentration and subsequent production of cyclic quanosine monophosphate (cGMP). The latter affects the balance of intracellular calcium concentration and, ultimately, the contractile activity of the cell. Our computations show, that cGMP-induced inhibition of Ca2 +-ATPase, localized (i) in the cell membrane or (ii) in the membrane of sarcoplasmic reticulum has a different effect on the characteristics of calcium oscillations and, therefore, potentially has a different relaxing effect.

Reference: 
  1. Фундаментальная и клиническая физиология / пер с англ. и нем. под ред. А. Камкина, А. Каменского. М. : Академия, 2004. 340 с.; 342 c
  2. Keener J., Sneyd J. Mathematical Physiology. N.Y. : Springer-Verlag, 1998. P. 163.
  3. Yang J., Clark J. W., Brayn R. M., Robertson C. S. Mathematical modeling of the nitric oxide/cGMP pathway in the vascular smooth muscle cell // Amer. J. Physiol. Heart Circ. Physiol. 2005. Vol. 289. H886–H897.
  4. Carvajal J. A., Germain A. M., Huidobro-Toro J. P., Weiner C. P. Molecular mechanism of cGMP-mediated smooth muscle relaxation // J. Cell Physiol. 2000. Vol. 184. P. 409–420.
  5. Lincoln T. M., Dey N., Sellak H. cGMP-dependent protein kinase signaling mechanisms in smooth muscle : from the regulation of tone to gene expression // J. Appl. Physiol. 2001. Vol. 91. P. 1421–1430.
  6. Lucas K. A., Pitari G. M., Kazerounian S., Ruiz-Stewart I., Park J., Schulz S., Chepenik K. P., Waldman S. A. Guanylyl ceclases and signaling by cyclic GMP // Pharmacological reviews. 2000. Vol. 52. P. 375–414.
  7. Houart G., Dupont G., Goldbeter A. Bursting, Chaos and Birhythmicity Originating from Self-modulation of the Inositol 1,4,5-trisphosphate Signal in a Model for Intracellular Ca2+ Oscillations // Bulletin of Mathematical Biology. 1999. № 61. P. 507–530.
  8. Dupont G., Goldbeter A. One-pool model for Ca2+ oscillations involving Ca2+ and inositol 1,4,5-triphosphate as co-agonist for Ca2+ release // Cell Calcium. 1993. № 14. P. 311–322.
  9. Takazawa K., Lemos M., Delvaux A., Lejeune C., Dumont J. E., Erneux C. Rat brain inositol 1,4,5-trisphosphate 3-kinase. Ca2+sensitivity, purifi cation and antibody production // Biochemical J. 1990. Vol. 268. P. 213–217.
  10. Takazawa K., Passareiro H., Dumont J.E., Erneux C. Purifi cation of bovine brain inositol 1,4,5-trisphosphate 3-kinase. Identifi cation of the enzyme by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis // Biochemical J. 1989. Vol. 261. P. 483–488.
  11. Berridge M. J. Inositol trisphosphate and calcium signaling // Nature. 1993. Vol. 361. P. 315–325.
  12. Nillson H., Aalkjar C.Vasomotion : Mechanisms and Physiological Importance // Molecular Interventions. 2003. № 3. P. 79–89.
  13. Bursztyn L., Eytan O., Jaffa A. J., Elad D. Mathematical model of excitation-contraction in a uterine smooth muscle cell // Amer. J. Physiol Cell. Physiol. 2007. № 292. P. 1816–1829.