## School of Veterinary Medicine, Department of Veterinary Science

八百坂紀子 ヤオサカ ノリコ

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Last Update :2019/05/22

### Researcher Profile and Settings

#### Name

YAOSAKA Noriko |

#### Affiliation (Master)

School of Veterinary Medicine, Department of Veterinary Science |

### Research Activities

#### Misc

デンタルケアの現状と口腔内衛生状況との関連, 大野愛満, 長谷川絢, 伊藤綾展, 郡山尚紀, 八百坂紀子, Veterinary Nursing, 21, 2016 06 20 , http://jglobal.jst.go.jp/public/201602233684464208 |

Regulation of heart contractility by M<inf>2</inf> and M<inf>3</inf> muscarinic receptors: Functional studies using muscarinic receptor knockout mouse, Takio Kitazawa, Hiroki Teraoka, Nao Harada, Kenta Ochi, Tatsuro Nakamura, Koichi Asakawa, Shinya Kanegae, Noriko Yaosaka, Toshihiro Unno, Sei Ichi Komori, Masahisa Yamada, Neuromethods, 107, 2016 01 01 , 10.1007/978-1-4939-2858-3_13, https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84938704876&origin=inward, © Springer Science+Business Media New York 2016. To investigate the functional roles of M < inf > 2 < /inf > and M < inf > 3 < /inf > muscarinic receptors in mouse atria, wild-type mice, muscarinic M < inf > 2 < /inf > or M < inf > 3 < /inf > single receptor knockout mice (M < inf > 2 < /inf > KO, M < inf > 3 < /inf > KO), and M < inf > 2 < /inf > and M < inf > 3 < /inf > muscarinic receptor double knockout mice (M < inf > 2 < /inf > /M < inf > 3 < /inf > KO) were used for pharmacological and molecular biological approaches. Effects of carbachol on spontaneous contraction (right atrium) or electrically evoked contraction (left atrium) were examined in the isolated atria of the respective mice. Presence of muscarinic receptor subtype mRNAs and proteins was determined by real time RT-PCR using specifi c primers and immunohistochemistry using specifi c anti-M < inf > 2 < /inf > and anti-M < inf > 3 < /inf > receptor antibodies. Quantitative real-time RT-PCR analysis showed that M 2 receptor mRNA was expressed dominantly in mouse atria but that the M < inf > 1 < /inf > , M < inf > 3 < /inf > , M < inf > 4 < /inf > , and M < inf > 5 < /inf > receptor subtypes were also expressed at low levels. Carbachol decreased the frequency of spontaneous beating in right atria of mice through activation of the M < inf > 2 < /inf > receptor subtype. In left atria of wild-type mice, carbachol decreased the amplitude of electrical field stimulation (EFS)-evoked contractions (M < inf > 2 < /inf > receptors), but this inhibition was transient and was followed by a gradual increase in contraction amplitude (M < inf > 3 < /inf > receptors). Cyclooxygenase-2 (COX-2) and prostaglandins in the endocardial endothelium were involved in the M < inf > 3 < /inf > receptor-mediated positive inotropic actions. In conclusion, the present studies using isolated atria of muscarinic receptor knockout mice demonstrated that myocardial M < inf > 2 < /inf > receptors mediate negative chronotropic/inotropic actions and that M < inf > 3 < /inf > muscarinic receptors mediate positive chronotropic/inotropic actions in mouse atria. Physiologically, M < inf > 3 < /inf > receptor-mediated excitatory cardiac effects might dampen the inhibitory effects of M < inf > 2 < /inf > receptor activation on cardiac contractility. |

Velpeauスリング法により整復が奏功した子牛の肩甲骨背側脱臼の1例, 平塚可弥乃, 草場綾乃, 嶋守俊雄, 八百坂紀子, 北澤多喜雄, 鈴木一由, 北海道獣医師会雑誌, 58, 2014 08 10 , http://jglobal.jst.go.jp/public/201402212784479934 |

北海道犬の精索に発生した肉腫の一例, 八百坂紀子, 寺澤元子, 近藤佑美, 佐野悠人, 長峯栄路, 河村芳朗, 平山和子, 松田一哉, 岡本実, 横田博, 北澤多喜雄, 谷山弘行, 日本獣医学会学術集会講演要旨集, 155th, 2013 03 04 , http://jglobal.jst.go.jp/public/201302238940170312 |

馬喉頭蓋下嚢胞の1例に関する病理組織学的検索, 遠藤ちひろ, 岡本実, 妙中友美, 河村芳朗, 近藤佑美, 油井武, 佐野悠人, 長峯栄路, 坂口佳菜子, 溝奥尋子, 平山和子, 松田一哉, 八百坂紀子, 谷山弘行, 日本獣医学会学術集会講演要旨集, 155th, 2013 03 04 , http://jglobal.jst.go.jp/public/201302292356748501 |

Immunohistochemical and functional studies for M 3 muscarinic receptors and cyclo-oxygenase-2 expressed in the mouse atrium, N. Harada, K. Ochi, N. Yaosaka, H. Teraoka, T. Hiraga, T. Iwanaga, T. Unno, S. Komori, M. Yamada, T. Kitazawa, T. Kitazawa, Autonomic and Autacoid Pharmacology, 32, 2012 10 01 , 10.1111/j.1474-8673.2012.00472.x, https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84866626652&origin=inward, In mouse atrium, M 2 and M 3 muscarinic receptors (M 2 R and M 3 R) are involved in biphasic (negative and positive) inotropic actions of muscarinic agonists, and the positive inotropic action is reduced by indomethacin. The aim of our study was to determine the localization of M 2 R, M 3 R and cyclo-oxygenase (COX) in mouse atrium and to characterize muscarinic receptor-mediated positive inotropy. M 2 R immunoreactivity was found only on atrial myocardium, but M 3 R immunoreactivity was localized on both the myocardium and endocardial endothelium. COX-1 and COX-2 immunoreactivities were identified in both myocardial and endocardial endothelium. In electrically stimulated left atria, carbachol caused M 2 R-mediated negative inotropy followed by M 3 R-mediated positive inotropy. Removal of atrial endothelium reduced the positive inotropy without affecting the negative inotropy, suggesting that stimulation of endothelial M 3 R mediates the positive inotropy. N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398, COX-2 inhibitor) decreased the carbachol-induced positive inotropy; however, 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-trifluoromethylpyrazole (SC560, COX-1 inhibitor), 1-[[4,5-bis(4-methoxyphenyl)-2-thiazolyl] carbonyl]-4-methylpiperazine (FR122047, COX-1 inhibitor) and l-nitroarginine meth ylester did not affect the inotropic response. M 3 R activation caused positive chronotropy in spontaneously beating right atria when M 2 R-mediated negative chronotropy was suppressed and rate of contraction was low, < 350 beats min -1 . Our results indicate that although M 3 Rs are located on both myocardial cells and endocardial endothelial cells, only endothelial M 3 Rs mediate positive inotropy in response to muscarinic agonists via activation of COX-2 in the mouse atrium. M 3 R-mediated positive chronotropy counteracting M 2 R-mediated negative chronotropy was also demonstrated. © 2012 Blackwell Publishing Ltd. |