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1996 Fiscal Year Final Research Report Summary

The role of intracellular Mg^<2+> and its mechanism in the regulation of cardiac Ca channels

Research Project

Project/Area Number 07670054
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field General physiology
Research InstitutionHIROSHIMA UNIVERSITY

Principal Investigator

YAMAOKA Kaoru  School of Medicine, HIROSHIMA UNIVERSITY Assistant Professor, 医学部, 講師 (10200586)

Project Period (FY) 1995 – 1996
KeywordsL-type Ca channel / frog / cardiac muscle / magnesium / calcium / GTP / phosphorylatioin
Research Abstract

This project revealed a great detail about action of intracellular Mg^<2+> on the L-type Ca channels in frog ventricular myocytes and indicated a physiological role of Mg^<2+> in the final step of the beta-adrenergic signal transduction pathway as follows.
1.Decrease in the concentration of intracelluar Mg^<2+> ([Mg^<2+>]_i) down to 1 muM resulted in increase in L-type Ca current (I_<Ca>) up to 10 times of the control. This was not mediated through phosphorylation nor GTP-binding protein but possibly by direct biding of Mg^<2+> to the channel. I_<Ca>- [Mg^<2+>]_i relationship was obtained and this relationship indicated that 80-90% of channels are inactivated under phsyiological [Mg^<2+>]_i.
2.Increase in the intracellular concentration of Ca^<2+> ([Ca^<2+>]_i) induce increase in I_<Ca>. This phenomenon is mediated through unblock of Mg^<2+> because Ca^<2+> competes for the site with Mg^<2+> and unbinds Mg^<2+>.
3.Increase in I_<Ca> by reducing [Mg^<2+>]_i was inhibited in the presence of intracellular GTP.This phenomenon has been shown for the first time. The inhibition by GTP was not mediated through GTP-binding protein but by its direct binding to the channel competetively with Mg^<2+>.
4.Phosphorylation of the L-type Ca channel altered the relationship between I_<Ca> and [Mg^<2+>]_i so that change in [Mg^<2+>]_i between 1muM and 1 mM did not induce change in I_<Ca> while I_<Ca> remained in the maximum value. This result provoked the idea that phosphorylation increases I_<Ca> by means of reducing the sensitivity of Ca channels to the blocking action of Mg^<2+> and, therefore, both channel phosphorylation and reduction of [Mg^<2+>]_i may share a common final step in modulation of the channel.

  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Yamaoka,K.: "Modulation of Ca2+ channels by intracellular Mg2+ ions and GTP in frog ventricular myocytes." Pflugers Arch. 432. 433-438 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yamaoka,K.: "Regulation of Ca channel by interacellular Ca2+ and Mg2+ in frog ventricular cells." Pflugers Arch. 431. 305-317 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yamaoka,K.: "A model of calcium-channel regulation by intracellular divalent cations for frog ventricular myocytes." Heart Vess. Supp19. 120-122 (1995)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yamaoka, K.and Seyama, I.: "Modulation of Ca^<2+> channels by intracellular Mg^<2+> ions and GTP in frog ventricular myocytes." Pflugers Arch.432. 433-438 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Yamaoka, K.and Seyama, I.: "Regulation of Ca channel by intracellular Ca^<2+> and Mg^<2+> in frog ventricular cells." Pflugers Arch.431. 305-317 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Yamaoka, K.: "A model of calcium-channel regulation by intracellular divalent cations for frog ventricular myocytes." Heart Vess.Suppl.9. 120-122 (1995)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 1999-03-09  

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