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Relationship between β-adrenergic signaling pathway and cytokines in hypertensive heart failure.

Research Project

Project/Area Number 10670689
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionKurume University

Principal Investigator

IWAMI Gensho  Kurume University, school of Medicine,Department of Medicine III, Assistant Professor, 医学部, 講師 (90203405)

Co-Investigator(Kenkyū-buntansha) KIKUCHI Toshio  Kurume University, school of Medicine,Department of Medicine III, Instructor, 医学部, 助手 (20289432)
OKA Naoki  Kurume University, school of Medicine,Department of Medicine III, Instructor, 医学部, 助手 (00299421)
西 宏文  久留米大学, 医学部, 講師 (60189248)
中田 真詩  久留米大学, 医学部, 講師 (70180304)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
Keywordsheart failure / β-adrenergic pathway / Adenylyl cyclase / cytokine / β-受容体 / アデニル酸シクラーゼ / β-受容体リン酸化酵素 / BNP / IGF-1
Research Abstract

[Purpose] The cardiac β-adrenergic pathway is downregulated in heart failure. There are conflicting reports about the change of down stream of β-adrenergic signaling pathways in heart failure. We examined βAR, adenylyl cyclase (AC), βAR kinase 1 (βARK 1) and G protein coupled receptor kinase (GRK5) in heart failure (HF) of Dahl salt-sensitive rats (DS). Also we examined how cytokines inhibited the cardiac β-adrenergic pathway.
[Result] Echocardiography showed that DS- fed an 8 % NaCl diet developed left ventricular (LV) hypertrophy at 18 wk, followed by marked LV systolic dysfunction. The HF rats had increased plasma norepinephrine associated with decrease of βAR. The amount of βARK 1 and GRK5 in cytosolic fraction were increased in the HF rats. AC activity of LV membrane fraction was decreased, and also northern blotting showed that AC type V mRNA was decreased in the HF rats. In the HF rats, cardiac lL-1β and TNFa were increased. Also in vitro lL-1 β and TNFα inhibited cardiac AC activities which stimulated by isoproterenol and GTPgS. However, AC activity stimulated by forskolin did not show any inhibition of lL-1β and TNFa.
[Conclusion] The data suggests that high salt diet causes hypertensive heart failure in DS by a mechanism which may involve down regulation of the pathway from down stream to β-adrenoceptor. And lL-1 β and TNFα may involve interaction between β-adrenoceptor and G-protein.

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] 岩見元照: "心筋症"臨床外科. 54. 419-421 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] 岩見元照: "心筋疾患と遺伝子異常"臨床検査. (印刷中).

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Iwami G: "Cardiomyopathies and gene mutations"Clinical Surgery. 54. 419-421 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] Iwami G and Koga Y: "Cardiomyopathies"Clinical Examination. 44(6)(in press). (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] 岩見元照: "心筋症"臨床外科. 54. 419-421 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] 岩見元照: "心筋疾患と遺伝子異常"臨床検査. (印刷中).

    • Related Report
      1999 Annual Research Report

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Published: 1998-04-01   Modified: 2016-04-21  

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