Українська English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2013; 59(3): 18-24

Ionic mechanisms of carbon monoxide action on the contractile properties of smooth muscles of the blood vessels

Baskakov MB1, Zheludeva AS1, Gusakova SV3, Smagliĭ LV3, Aleĭnik AN3, Ianchuk PI2, Medvedev MA1, Orlov SN2

  1. Siberian State Medical University, Tomsk, Russia;Tomsk Polytechnic University, Russia;
  2. Laboratory of the Research Center of the University of Montreal, Canada;
  3. Taras Shevchenko National University of Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz59.03.018


Abstract

Carbon monoxide (CO) is one of a family of gas transmitters. In this article we present the results of mechanographic investigations of the mechanisms of CO action on a rat thoracic aorta segments. We found that relaxing effect of CO donor CORM-2 on vascular smooth muscles is mediated mainly by opening of voltage-dependent potassium channels in smooth muscle cells: 4-aminopyridine, blocking these channels, almost completely eliminated the CO-induced vasorelaxation of the segments precontracted by depolarization of the smooth muscle cells membranes with high potassium (30 mM KCl) solution or by phenylephrine (10 microM). For the first time we documented that CORM-2 reduces the nicardipine-sensitive input of 45Ca2+ in freshly isolated aorta cells. There are reasons to suggest that the L-type voltage-dependent calcium channels of vascular smooth muscle cells are another target for CO, which is implemented in the relaxing effect of this gas transmitter. Additional research is needed to determine the influence of ruthenium complexes (Ru(II)) on phenomenology of carbon monoxide effects.

Keywords: carbon monoxide, vascular smooth muscles,potassium channels, L-type calcium channels

Full text: (PDF, in Russian)

References

  1. Adams D.J., Hill M.A. Potassium channels and membranepotential in the modulation of intracellular calcium invascular endothelial cells . J. Cardiovasc. Electrophysiol.2004. 15. R.598-610.
    2.  
  2. Baskakov M., Gusakova S., Smagly L. Mechanismsof regulation of gasotransmitters contractile activity ofsmooth muscle cells . Hypertension. 2012. 30. Suppl.A. P. 366.
    3.  
  3. Burnham M., Bychkov R. Characterization of an apaminsensitivesmallconductance Ca2+ activated K+ channels inporcine coronary artery endothelium: relevance to EDHF. Br J. Pharmacol. 2002. 135. P.1133-1143. CrossRef PubMed PubMedCentral
    4.  
  4. Catterall W.A. Structure and regulation of voltage-gatedCa2+-channels . Annu Rev. Cell. Dev. Biol. 2000. 16.P.521-555. CrossRef PubMed
    5.  
  5. Gagov H., Kadinov B., Christov K. Role of constitutivelyexpressed heme-oxiginase-2 in the regulation of guineapig coronary artery tone . Pflueg. Arch. Eur. J. Physiol. 2003. 446. P.412-421. CrossRef PubMed
    6.  
  6. Jaggar J.H., Leffler C.W., Cheranov S.Y. Carbon monoxidedilates cerebral arterioles by enhancing the coupling ofCa2+ sparks to Ca2+-activated K+ channels . Circ. Res. 2002. 91, N 7. P.610-617. CrossRef PubMed
    7.  
  7. Jaggar J., Li A., Parfenova H. Heme is a carbon monoxidefor large-conductance Ca2+-activated K+ channels. Circ Res. 2005. 97, N 8. P.805-812. CrossRef PubMed PubMedCentral
    8.  
  8. Kamp T.J., Hell J.W. Regulation of cardiac L-type calciumchannels by protein kinase A and protein kinase C . Circ.Res. 2000. 87, N 12. P.1095-102. CrossRef PubMed
    9.  
  9. Monaghan A.S. Benton D.C, Bahia P.K, Hosseini R, ShahY.A, Haylett D.G, Moss G.W. The SK3 subunit of smallconductance Ca2+-activated K+ channels interacts withboth SK1 and SK2 subunits in a heterologous expressionsystem . J.Biol. Chem.2004. 279. P.1003-1009. CrossRef PubMed
    10.  
  10. Motterlini R., Clark J., Foresti R. Carbon Monoxide releasing molecules: characterization of biochemical andvascular activities . Cerculation Research. 2002. 90.P.17-24. CrossRef  
  11. Motterlini R. Carbon monoxide-releasing molecules (CORMs):anti-ischaemic and anti-inflammatoryactivities . Biochemical Society Transactions. 2007. 35, N5. P.1142-1146. CrossRef PubMed
    12.  
  12. Orlov S.N., Tremblay J. cAMP signaling inhibitsdihydropyridine-sensitive Ca2+ influx in vascular smoothmuscle cells . Hypertension. 1996. 27. P.774-780. CrossRef PubMed
    13.  
  13. Sansom M.S.P., Shrivastava I.H., Bright J.N. et al. mPotassium channels: structures, models, simulations . Biochemica et Biophysica Acta. 2002. 1565. P.294-307. CrossRef  
  14. Sheng J.Z., Andrew P.B Smalland intermediateconductance Ca2+-activated K+ channels directly control agonist-evoked nitric oxide synthesis in human vascular endothelial cells . Amer. J. Cell. Physiol. 2007. 293. P.458-467. CrossRef PubMed
    15.  
  15. Tang X.D., Xu R., Reynolds M.F. Haem can bind to and inhibit mammalian calcium-dependent Slo1 BK channels . Nature. 2003. 425. P.531-535. CrossRef PubMed
    16.  
  16. Williams J. The functions of two species of calcium channel in cardiac muscle excitation-contraction coupling . European Heart Journal. 1997. 18. P.A27-A35. CrossRef PubMed
    17.  
  17. Wilkinson W.J., Kemp P.J. Carbon monoxide: an emerging regulator of ion channels . J. Physiol. 2011. 589. P.3055-3062. CrossRef PubMed PubMedCentral
    18.  
  18. Wu L., Wang R. Carbon monoxide: endogenous production, physiological functions, and pharmacological applications . Pharmacol. Rev. 2005. 57. P.585-630. CrossRef PubMed
    19.  
  19. Wu L., Cao K., Lu Y., Wang R. Different mechanisms underlying the stimulation of KCa channels by nitric oxide and carbon monoxide . J. Clin Invest. 2002. 110. P. 691-700. CrossRef PubMed PubMedCentral
    20.    

© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2024.