Differential Contribution of Nerve-Derived Noradrenaline to High K⁺-Induced Contraction Depending on Type of Artery

• Ishida Hirotake

  Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka

• Saito Shin-ya

  Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka

• Hishinuma Eita

  Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka

• Ishikawa Tomohisa

  Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka

書誌事項

タイトル別名

• Differential Contribution of Nerve-Derived Noradrenaline to High K⁺-Induced Contraction Depending on Type of Artery

抄録

High K⁺-induced contraction of arterial smooth muscle is thought to be mediated by membrane depolarization and subsequent activation of voltage-dependent Ca²⁺ channels (VDCCs). In line with this, this study found that contraction induced by 80 mM K⁺ was almost abolished by nifedipine (1 µM), a VDCC inhibitor, in isolated rat aorta, and was markedly suppressed in the iliac artery. However, nifedipine (1 µM) only partially suppressed high K⁺-induced contraction in the tail artery. The contractions remaining in the arteries were further reduced by non-selective cation channel (NSCC) inhibitors, including 2-aminoethoxydiphenyl borate (2-APB) (100 µM), SK&F96365 (10 µM), and 3,4-dihydro-6,7-dimethoxy-α-phenyl-N,N-bis[2-(2,3,4-trimethoxyphenyl)ethyl]-1-isoquinolineacetamide hydrochloride (LOE908) (10 µM). In particular, sustained tonic contraction was nearly abolished. Prazosin (0.3 µM), an α₁-adrenoceptor antagonist, partially inhibited high K⁺-induced contraction in the tail and iliac arteries, but had no effect in the aorta. Consistently, tyramine potently induced contraction in the tail and iliac arteries, but not in the aorta. Furthermore, the inhibition by prazosin and NSCC inhibitors of the high K⁺-induced contraction in the presence of nifedipine was comparable. These results suggest that depending on the type of artery, high K⁺-induced contraction is mediated by Ca²⁺ influx not only through VDCCs but also through NSCCs, the activation of which is due to the activation of α₁-adrenoceptors by the released noradrenaline from sympathetic nerve terminals resulting from high K⁺ stimulation.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 40 (1), 56-60, 2017

  公益社団法人 日本薬学会

キーワード

• high K⁺
• tail artery
• non-selective cation channel
• voltage dependent calcium channel
• noradrenaline

詳細情報

• CRID: 1390282679609540352
• NII論文ID: 130005188890
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.b16-00590
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 027818839
• PubMed: 28049949
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I027818839
• Web Site: https://www.jstage.jst.go.jp/article/bpb/40/1/40_b16-00590/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2017254539
• 本文言語コード: en
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
  • KAKEN
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