R-(-)-α-methylhistamine, a histamine H3 receptor agonist, induces endothelium-dependent vasodilation in rat mesenteric resistance arteries

• Sun Pengyuan

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

• Jin Xin

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

• Koyama Toshihiro

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

• Li Simin

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

• Kitamura Yoshihisa

  Department of Pharmaceutical Care and Health Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

• Kawasaki Hiromu

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

書誌事項

タイトル別名

• R-(-)-.ALPHA.-Methylhistamine, a Histamine H3 Receptor Agonist, Induces Endothelium-Dependent Vasodilation in Rat Mesenteric Resistance Arteries
• R a methylhistamine a histamine H3 receptor agonist induces endothelium dependent vasodilation in rat mesenteric resistance arteries

抄録

A novel histamine receptor subtype, histamine H₃ receptor, mediates inhibition of peripheral autonomic neurotransmission. The present study was designed to examine vascular effects of histamine H₃ receptor by using a selective histamine H₃ receptor agonist, R-(−)-α methylhistamine (α-methylhistamine), in rat mesenteric resistance arteries. The isolated mesenteric vascular beds were perfused with Krebs solution and perfusion pressure was measured. Active tone was produced by perfusion of Krebs solution containing 7 μM methoxamine. In preparations with intact endothelium, perfusion of α-methylhistamine (1—100 μM) for 1 min produced a concentration-dependent vasodilation. The maximum vasodilation at the highest concentration was approximately 45%. This vasodilation was abolished by endothelium removal and attenuated by histamine H₃ receptor antagonists, thioperamide and clobenpropit, but not by chlorpheniramine (histamine H₁ receptor antagonist) and cimetidine (histamine H₂ receptor antagonist). N^ω-nitro-L-arginine methyl ester (L-NAME, nitric oxide (NO) synthase inhibitor), indomethacin (cyclooxygenase inhibitor) and tetraethylammonium (nonselective K⁺-channel blocker) and high KCl (30 mM) significantly inhibited α-methylhistamine-induced endothelium-dependent vasodilation. These findings suggest that α-methylhistamine induces endothelium-dependent vasodilation mainly via endothelium histamine H₃ receptors. It is also suggested that activation of histamine H₃ receptors in the endothelium releases mainly NO and partially prostaglandin I₂ and endothelium-derived hyperpolarizing factors to induce endothelium-dependent vasodilation.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 33 (1), 58-63, 2010

  公益社団法人 日本薬学会

キーワード

• histamine H₃ receptor
• endothelium-dependent vasodilation
• rat mesenteric artery
• endothelium-derived relaxing factor
• endothelium-derived hyperpolarizing factor

詳細情報

• CRID: 1390282679602480256
• NII論文ID: 130000140192
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.33.58
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 10497330
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I10497330
• Web Site: http://www.jstage.jst.go.jp/article/bpb/33/1/33_1_58/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2010153076
• 本文言語コード: en
• データソース種別:
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