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The new pathophysiological role and its mechanism of angiotensin receptor

Research Project

Project/Area Number 17590052
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Biological pharmacy
Research InstitutionTakasaki University of Health and Welfare (2006)
Tohoku University (2005)

Principal Investigator

YOSHIDA Makoto  Takasaki University of Health and Welfare, Faculty of Pharmacy, Professor, 薬学部, 教授 (90201011)

Co-Investigator(Kenkyū-buntansha) NAKAHATA Norimichi  Tohoku University, Graduate School of Pharmaceutical Sciences, Professor, 大学院・薬学研究科, 教授 (60045804)
HONMA Shigeyoshi  Takasaki University of Health and Welfare, Faculty of Pharmacy, Research instructor, 薬学部, 助手 (20344682)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
KeywordsAngiotensin / Pharmacology / Physiology
Research Abstract

To investigate the new pathophysiological role and its mechanisms of angiotensin type 1 receptor (AT1R) and angiotensin type 2 receptor (AT2R), we used MDCKII cell, a renal epithelial cell line, and PC-12 cell, a pheochromocytoma cell. In MDCKII cell stably transfected with rat AT2R, the stimulation with angiotensin II (Ang II) inhibited forskolin-induced cyclic AMP accumulation with dose-dependent manner. This inhibition was abolished by co-treatment with PD123319, a AT2R antagonist, or pre-treatment of pertussis toxin, suggesting the perticipation of the Gi protein-coupled mechanism of AT2R stimulation. The stimulation of this cell with Ang II under treatment AT1R antagonist activated the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2. Ang II reduced mRNA and protein level of AT2R in PC-12 cells transiently expressed rat AT1R. Double transfection of AT1AR and AT2R on PC-12 cells induced the Ang II-induced internalization of AT2R. These results suggest that 1) AT2R affect cell growth through activation of ERK 1/2 with Gi protein-coupled mechanism, 2) AT1R affect the AT2R expression with some unknown mechanism. Based on these results, further investigations using whole animal should be needed for clarify the pathophysiological role of AT2R.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (1 results)

All 2007

All Journal Article (1 results)

  • [Journal Article] Distinct effects of Z-335, a new thromboxane A2 receptor antagonist, on rabbit platelets and aortic smooth muscle.2007

    • Author(s)
      Yoshida M et al.
    • Journal Title

      Pharmacology 79

      Pages: 50-56

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Annual Research Report 2006 Final Research Report Summary

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Published: 2005-04-01   Modified: 2016-04-21  

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