Current Perspective : The Mechanism of Calcitonin Gene-Related Peptide-Containing Nerve Innervation

• Hashikawa-Hobara Narumi

  Department of Life Science, Okayama University of Science, Japan Department of Life Science, Okayama University of Science, Japan

• Hashikawa Naoya

  Department of Life Science, Okayama University of Science, Japan Department of Life Science, Okayama University of Science, Japan

• Zamami Yoshito

  Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan

• Takatori Shingo

  Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan

• Kawasaki Hiromu

  Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Japan

書誌事項

タイトル別名

• The Mechanism of Calcitonin Gene-Related Peptide–Containing Nerve Innervation
• The Mechanism of Calcitonin Gene-Related Peptide^|^ndash;Containing Nerve Innervation

抄録

Calcitonin gene-related peptide (CGRP) is a major neurotransmitter and CGRP-containing primary sensory neurons play an important role in nociception and potent vasodilation. CGRP-containing nerves in mesenteric arteries are decreased in pathological animal models (hypertension, diabetes, and atherosclerosis). In apolipoprotein E–knockout mice, which have atherosclerosis and peripheral sensory nerve defects, nerve growth factor (NGF)-mediated CGRP nerve facilitation was down-regulated, which may have been caused by the impairment of the Akt–NO–cGMP pathway. In addition, NGF-mediated CGRP neurite outgrowth was decreased in fructose-induced insulin-resistant rats. We recently discovered that renin–angiotensin inhibitors improved CGRP innervation in spontaneously hypertensive rats, indicating that rescuing CGRP nerve innervation might improve pathophysiological conditions. To find a novel reagent that facilitates CGRP nerves, a new model, phenol-injured perivascular nerve model rats, was established. Adrenomedullin, hepatocyte growth factor, and angiotensin II type 2 receptor activation induced CGRP nerve distribution in phenol-injured rats. Furthermore, in insulin-resistant model rats, the down-regulation of CGRP nerves was likely due to the depression of phosphoinositide 3-kinase (PI3K)-dependent Akt activation. Administration of candesartan improves CGRPergic function via the PI3K–Akt pathway in insulin-resistant rats. Thus, clarification of the mechanisms of CGRP nerve defects may constitute future therapeutic targets.

収録刊行物

• Journal of Pharmacological Sciences

  Journal of Pharmacological Sciences 119 (2), 117-121, 2012

  公益社団法人 日本薬理学会

キーワード

• calcitonin gene-related peptide–containing nerve
• nerve growth factor–mediated neurite outgrowth
• angiotensin II type 2 receptor
• PI3K–Akt pathway

詳細情報

• CRID: 1390001205180041344
• NII論文ID: 10030828329
• NII書誌ID: AA11806667
• DOI: 10.1254/jphs.12r02cp
• COI: 1:CAS:528:DC%2BC38XpsV2jtrs%3D
• ISSN: 13478648
• ISSN: 13478613
• NDL書誌ID: 023750705
• PubMed: 22673132
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I023750705
• Web Site: https://search.jamas.or.jp/link/ui/2013106967
• 本文言語コード: en
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可