European Journal of Biophysics

| Peer-Reviewed |

Age-Dependent Impairment of Heart Muscle Contractility as a Primary Mechanism for Overexpression of Na+/Ca2+ Exchanger in Brain Cortex Tissues

Received: 19 July 2019    Accepted: 15 August 2019    Published: 29 August 2019
Views:       Downloads:

Share This Article

Abstract

The cognitive function of brain and contractility of heart muscle are accompanied with age-dependent dehydration of tissues of these two organs. The aim of the present study is to reveal which of the abovementioned two organs primarily fail as a result of dysfunction of age-sensitive metabolic mechanism. For this purpose, the age-dependent sensitivity of cell hydration in brain cortex and heart muscle tissues are studied through depressing metabolic activity by cooling and its activation by supplying animals with distilled water, by inactivation of Na+/K+ pump and activation of Na+/Ca2+ exchange in the reverse mode. The obtained data bring us to the conclusion that the metabolic regulation of brain cortex and heart muscle tissues has different nature. The age-dependent dysfunction of Na+/K+ pump–induced activation of RNa+/Ca2+ exchange leads to dysfunction of heart muscle contractility because of activation of Ca-calmoduline-NO-cGMP production, which brings to FNa+/Ca2+ exchange induced muscle relaxation and it could serve as a primary mechanism for dysfunction of brain tissues’ metabolic control of cell hydration, which leads to overexpression of Na+/Ca2+ exchanger in the membrane.

DOI 10.11648/j.ejb.20190702.11
Published in European Journal of Biophysics (Volume 7, Issue 2, December 2019)
Page(s) 27-42
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Hydration, Brain Cortex, Heart Muscle, [3H]-Ouabain, Na+/K+ Pump

References
[1] Ayrapetyan S. N., Suleymanyan M. A., Sagian A. A. and Dadalyan S. S. (1984). Autoregulation of electrogenic sodium pump. Cel. Mol. Neurobiol, 4, 367–384.
[2] Ayrapetyan S. N., Arvanov V. L., Maginyan S. B. and Azatyan K. V. (1985). Further study of the correlation between Na-pump activity and membrane chemosensitivity. Cell. Mol. Neurobiol, 5 (3), 231-243.
[3] Ayrapetyan S. N., Rychkov G. Y. and Suleymanyan M. A. (1988). Effects of water flow on transmembrane ionic currents in neurons of Helix pomatia and in Squid giant axon. Comp. Biochem Physiol, 89A, 179-186.
[4] Parton R. and Simons K. (2007). The multiple faces of caveolae. Nature Rev, 8 (3), 185-194.
[5] Parsegian V. A, Rand R. P. and Rau D. C. (2000). Osmotic stress, crowding, preferential hydration, and binding: a comparison of perspectives. Proc Natl Acad Sci USA, 97, 3987-3992.
[6] Ayrapetyan G., Grogoryan A., Dadasyan E. and Ayrapetyan S. (2007). The comparative study of the effect of 4Hz electromagnetic fields, infrasound- treated and hydrogen peroxide containing physiological solutions on Na pump- induced inhibition of heart muscle contractility. The Environmentalist, 27 (4), 483-488.
[7] Kojima M., Ayrapetyan S. and Koketsu K. (1984). On the membrane potential independent mechanism of sodium pump-induced inhibition of spontaneous electrical activity of Japanese land snail neurons. Comp Biochem Physiol, 77, 577-583.
[8] Ayrapetyan S. N., Grigorian K. V., Avanesyan A. S. and Stamboltsian K. V. (1994). Magnetic fields alter electrical properties of solutions and their physiological effects. Bioelectromagnetics, 15 (2), 133-142.
[9] Kazaryan S., Grigoryan K., Ayrapetyan S. and Mndzhoyan O. (1995). Derivatives of natural amino acids as radioprotectors. Pharmaceutical Chemistry Journal, 29 (7), 11-15.
[10] Baker P. F., Blaustein M. P., Hodgkin A. L. and Steinhardt S. A. (1969). The influence of Ca on Na efflux in squid axons. J Physiol, 200, 431-458.
[11] Blaustein M. P., Zhang J., Chen L., Song H., Raina H., Kinsey S. P., Izuka M., Iwamoto T., Kotlikoff M. I., Lingrel J. B., Philipson K. D., Wier W. G. and Hamlyn J. M. (2009). The Pump, the Exchanger, and Endogenous Ouabain: signaling mechanisms that link salt retention to hypertension. Hypertension, 53, 291-298.
[12] Saghian, A. A., Ayrapetyan, S. N. and Carpenter, D. O. (1996) Low concentrations of ouabain stimulate Na/Ca exchange in neurons. Cell Mol Neurobiol, 16, 180-185.
[13] Ayrapetyan, S. N. and Carpenter, D. O. (1991a). Very Low Concentrations of Acetylcholine and GABA Modulate Transmitter Responses. Neuroreport, 2, 563-565.
[14] Ayrapetyan S. N. and Carpenter D. O. (1991b). The Modulatory Effect of Extremely Low Doses of Mediators on Functional Activity of the Neuronal Membrane. Zh Evol Biokhim Fiziol, 27, 146-151 (in Russian).
[15] Ayrapetyan S. (2017). The intracellular signaling system controlling cell hydration as a biomarker for EMF dosimetry, Dosimetry in Bioelectromagnetics, (ed. by M. Markov), USA: CRC Press, pp. 339-368.
[16] Heqimyan A., Narinyan L., Nikoghosyan A. and Ayrapetyan S. (2015). Age-dependent magnetic sensitivity of brain and heart muscles, Electromagnetic Fields in Biology and Medicine, (ed. by M. Markov), USA: CRC Press, pp. 217-230. http://dx.doi.org/10.1201/b18148-15.
[17] Nikoghosyan A., Heqimyan A. and Ayrapetyan S. (2016). Primary mechanism responsible for age-dependent neuronal dehydration. International Journal of Basic and Applied Sciences, 5 (1), 5-14.
[18] Narinyan L., and Ayrapetyan S. (2015). Dysfunction of nM ouabain-induced activation of the signaling system responsible for age-related heart muscle failure. Advances in Life Sciences, 5 (4), 73-84.
[19] Adams H. R, Parker J. L and Mathew B. P. (1977). The influence of ketamine on inotropic and chronotropic responsiveness of heart muscle. J Pharmacol Exp Ther, 201 (1), 171-183.
[20] Akbar L., Sarioğlu Y. and Utkan T. (1992). Effect of ketamine on contractile performance of isolated frog myocardium and comparison of ketamine, thiopental and droperidol. Mater Med Pol, 24 (1), 32-34.
[21] Takahashi R. and Aprison M. 1964. Acetylcholine content of discrete areas of the brain obtained by a near-freezing method. J Neurochem 11, 887-892.
[22] Adrian R. H. (1956). The effect of internal and external K concentration on the membrane potential of frog muscle. J Physiol (Lond), 133, 631-658.
[23] Baker P. F. and Willis J. S. 1972. Binding of cardiac glycoside ouabain to intact cells. J Physiol 224, 441-462.
[24] Narinyan L. and Ayrapetyan S. (2017). Cyclic AMP-dependent signaling system is a primary metabolic target for non-thermal effect of microwaves on heart muscle hydration. Electromagn Biol Med, 32 (2), 182-191.
[25] Brini M. and Carifolly E. (2009). Calcium pumps in health and disease. Physiol Rev, 89, 1341-1378.
[26] Lehninger A. L. (1970). Mitochondria and calcium ion transport. Biochem J, 119, 129-138.
[27] Narinyan L., Ayrapetyan G. and Ayrapetyan S. (2012). Age-dependent magnetosensitivity of heart muscle hydration. Bioelectromagnetics, 33 (6), 452-458.
[28] Ayrapetyan S. N., Heqimyan A. A. and Nikoghosyan A. K. (2012). Age-dependent brain tissue hydration, Ca exchange and their dose-dependent ouabain sensitivity. J Bioequiv Availab, 4, 060-068.
[29] Khachaturian Z. S. (1989). The Role of Calcium Regulation in Brain Aging: Reexamination of a Hypothesis. Aging, 1, 17-34.
[30] Azatian K., White A., Walker R. and Ayrapetyan S. (1998). Cellular and molecular mechanisms of nitric oxide-induced heart muscle relaxation. Gen Pharmacol, 30 (4), 543-553.
[31] Narinyan L. and Ayrapetyan S. (2015). Dysfunction of nM ouabain-induced activation of the signaling system responsible for age-related heart muscle failure. Advances in Life Sciences, 5 (4), 73-84.
Author Information
  • Life Sciences International Postgraduate Educational Center, Unesco Chair in Life Sciences, Yerevan, Armenia

  • Life Sciences International Postgraduate Educational Center, Unesco Chair in Life Sciences, Yerevan, Armenia

Cite This Article
  • APA Style

    Lilia Narinyan, Sinerik Ayrapetyan. (2019). Age-Dependent Impairment of Heart Muscle Contractility as a Primary Mechanism for Overexpression of Na+/Ca2+ Exchanger in Brain Cortex Tissues. European Journal of Biophysics, 7(2), 27-42. https://doi.org/10.11648/j.ejb.20190702.11

    Copy | Download

    ACS Style

    Lilia Narinyan; Sinerik Ayrapetyan. Age-Dependent Impairment of Heart Muscle Contractility as a Primary Mechanism for Overexpression of Na+/Ca2+ Exchanger in Brain Cortex Tissues. Eur. J. Biophys. 2019, 7(2), 27-42. doi: 10.11648/j.ejb.20190702.11

    Copy | Download

    AMA Style

    Lilia Narinyan, Sinerik Ayrapetyan. Age-Dependent Impairment of Heart Muscle Contractility as a Primary Mechanism for Overexpression of Na+/Ca2+ Exchanger in Brain Cortex Tissues. Eur J Biophys. 2019;7(2):27-42. doi: 10.11648/j.ejb.20190702.11

    Copy | Download

  • @article{10.11648/j.ejb.20190702.11,
      author = {Lilia Narinyan and Sinerik Ayrapetyan},
      title = {Age-Dependent Impairment of Heart Muscle Contractility as a Primary Mechanism for Overexpression of Na+/Ca2+ Exchanger in Brain Cortex Tissues},
      journal = {European Journal of Biophysics},
      volume = {7},
      number = {2},
      pages = {27-42},
      doi = {10.11648/j.ejb.20190702.11},
      url = {https://doi.org/10.11648/j.ejb.20190702.11},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.ejb.20190702.11},
      abstract = {The cognitive function of brain and contractility of heart muscle are accompanied with age-dependent dehydration of tissues of these two organs. The aim of the present study is to reveal which of the abovementioned two organs primarily fail as a result of dysfunction of age-sensitive metabolic mechanism. For this purpose, the age-dependent sensitivity of cell hydration in brain cortex and heart muscle tissues are studied through depressing metabolic activity by cooling and its activation by supplying animals with distilled water, by inactivation of Na+/K+ pump and activation of Na+/Ca2+ exchange in the reverse mode. The obtained data bring us to the conclusion that the metabolic regulation of brain cortex and heart muscle tissues has different nature. The age-dependent dysfunction of Na+/K+ pump–induced activation of RNa+/Ca2+ exchange leads to dysfunction of heart muscle contractility because of activation of Ca-calmoduline-NO-cGMP production, which brings to FNa+/Ca2+ exchange induced muscle relaxation and it could serve as a primary mechanism for dysfunction of brain tissues’ metabolic control of cell hydration, which leads to overexpression of Na+/Ca2+ exchanger in the membrane.},
     year = {2019}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Age-Dependent Impairment of Heart Muscle Contractility as a Primary Mechanism for Overexpression of Na+/Ca2+ Exchanger in Brain Cortex Tissues
    AU  - Lilia Narinyan
    AU  - Sinerik Ayrapetyan
    Y1  - 2019/08/29
    PY  - 2019
    N1  - https://doi.org/10.11648/j.ejb.20190702.11
    DO  - 10.11648/j.ejb.20190702.11
    T2  - European Journal of Biophysics
    JF  - European Journal of Biophysics
    JO  - European Journal of Biophysics
    SP  - 27
    EP  - 42
    PB  - Science Publishing Group
    SN  - 2329-1737
    UR  - https://doi.org/10.11648/j.ejb.20190702.11
    AB  - The cognitive function of brain and contractility of heart muscle are accompanied with age-dependent dehydration of tissues of these two organs. The aim of the present study is to reveal which of the abovementioned two organs primarily fail as a result of dysfunction of age-sensitive metabolic mechanism. For this purpose, the age-dependent sensitivity of cell hydration in brain cortex and heart muscle tissues are studied through depressing metabolic activity by cooling and its activation by supplying animals with distilled water, by inactivation of Na+/K+ pump and activation of Na+/Ca2+ exchange in the reverse mode. The obtained data bring us to the conclusion that the metabolic regulation of brain cortex and heart muscle tissues has different nature. The age-dependent dysfunction of Na+/K+ pump–induced activation of RNa+/Ca2+ exchange leads to dysfunction of heart muscle contractility because of activation of Ca-calmoduline-NO-cGMP production, which brings to FNa+/Ca2+ exchange induced muscle relaxation and it could serve as a primary mechanism for dysfunction of brain tissues’ metabolic control of cell hydration, which leads to overexpression of Na+/Ca2+ exchanger in the membrane.
    VL  - 7
    IS  - 2
    ER  - 

    Copy | Download

  • Sections