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PHYSIOLOGICAL SIGNIFICANSE OF THE PATHWAY OF MONOVALENT CATIONS ON THE Ca STORES IN THE INTRACELLULAR SIGNAL TRANSDUCTION OF VASCULAR CELLS

Research Project

Project/Area Number 05837017
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field 血管生物学
Research InstitutionKYUSHU UNIVERSITY

Principal Investigator

YAMAMOTO Hiromichi  KYUSHU UNIV.FACULTY OF MEDICINE RESEARCH ASSOCIATE, 医学部, 助手 (20166820)

Project Period (FY) 1993 – 1994
Project Status Completed (Fiscal Year 1994)
Budget Amount *help
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
KeywordsVascular cells / Calcium ion / Monovalent ions / Signal transduction
Research Abstract

1.ATP-dependent ^<45>Ca^<2+> uptake into and efflux from intracellular Ca^<2+> stores were measured in saponin-skinned smooth muscle cells which were primary cultured from the rat aorta.
2.When 130 mM KC1 of the buffer solution was substituted for LiC1, Tris・HC1, NH4C1, choline chloride or sucrose, the efflux rate increased. However, it did not change in case of RbC1, CsC1 and NaC1. Valinomycin either inhibited or modified these changes. These results suggested that there exist potential-sensitive Ca^<2+> release channels on the membrane of the stores and that they were opened by the substitution of KC1 for impermeable monovalent cations.
3.When KC1 was substituted for choline chloride, Tris・HC1, LiC1, ^<45>Ca^<2+> uptake was inhibited remarkably. It was suggested that inhibitory effects of these cations on potassium efflux from the stores possibly suppressed Ca^<2+> uptake.
4.Effects of substitution on KC1 for vharious monovalent cations or sucrose on inositol tris phosphate-induced Ca^<2+> release (IICR) were examined in the presence and absence of 300 nM Ca^<2+>. From the magnitude of inhibition of IICR caused by the substitution of KC1, it was able to estimate changes in membrane potential and, hence, an order of relative permeability of monovalent cations.
5.Effects of substitution of KC1 for various monovalent cations or sucrose on Ca^<2+>-or caffieine-induced Ca^<2+> release (CICR) were examined. It was shown that the substitution of KC1 might have changed membrane potential to become negative inside the store and inhibited CICR.However, unlike IICR,it was also suggested that Ca^<2+> itself could give influence to cation-permeable channels.
6.In conclusion, it was suggested that Ca^<2+> uptake into and release from the intracellular stores in rat aortic smooth muscle cells were regulated by the movement of monovalent cations through the membrane of the stores.

Report

(3 results)
  • 1994 Annual Research Report   Final Research Report Summary
  • 1993 Annual Research Report
  • Research Products

    (11 results)

All Other

All Publications (11 results)

  • [Publications] Mayuko,Kodama: "Myosin Phosphorylation and Ca^<2+> sensitization in porcine cordnary arteridl smooth muscle stimulated with endothelin-1" European Journal of Pharmacology(Molecula pharmacology section). 288. 69-77 (1994)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1994 Final Research Report Summary
  • [Publications] Hiromichi,Yamamoto: "The substitution of impermeant monovalent cations for K^+ induces the Ca^<2+> release from the intracellulor,stores in rat adrtic smooth muscle cells" Pflugers Archives European J Physiology. (発表予定). (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1994 Final Research Report Summary
  • [Publications] 山本博道(分担): "血管の分子生物学" メディカル・レビュー社, (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1994 Final Research Report Summary
  • [Publications] Yamamoto, H.: "The substitution of impermeant monovalent cations for K+ induced the Ca2+ release from the intracellular stores in rat aortic smooth muscle cells." Pflugers Archives European J Physiology.(1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1994 Final Research Report Summary
  • [Publications] Kodama, M.: "Myosin phosphorylation and Ca2+ sensitization in porcine coronary arterial smooth muscle stimulated with endothelin-1." European Journal of Pharmacology.288. 69-77 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1994 Final Research Report Summary
  • [Publications] Yamamoto, H.: "Ca regulation of contraction and relaxation of vascular smooth muscle." Molecular biology of vessels. Medical Review.(1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1994 Final Research Report Summary
  • [Publications] Mayuko,Kodama: "Myosin phosphory lation and Ca^<2+> seusitization in porcine coronary artarial smooth muscle stimulated with endothelin‐1" European Journal of Pharmacology(Molecular Pharmacclosy section). 288. 69-77 (1994)

    • Related Report
      1994 Annual Research Report
  • [Publications] 山本博道(分担): "血管の分子生物学" メディカル レビュー社(発表予定), (1995)

    • Related Report
      1994 Annual Research Report
  • [Publications] Chiaki Watanabe: "Extra cellular Ca^<2+>-dependent potentiation by cocaine of serotonin-and norepinephrine-induced contractions in rat vascular smooth muscle" Circulation Research. 72. 1191-1201 (1993)

    • Related Report
      1993 Annual Research Report
  • [Publications] Chiaki Watanabe: "Mechanisms of caffeine-induced contraction and relaxation of rat aortic smooth muscle" Journal of Physiology. 456. 193-213 (1992)

    • Related Report
      1993 Annual Research Report
  • [Publications] 山本 博道: "血管平滑筋収縮弛緩のカルシウム制御" 血管と内皮. 3. 375-381 (1993)

    • Related Report
      1993 Annual Research Report

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Published: 1993-04-01   Modified: 2016-04-21  

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