WADA Tetsuyuki

WADA Tetsuyuki
Associate Professor
Faculty Department of Pharmacy / Graduate School of Medicine / Atomic Energy Research Institute

Education and Career


  • Kindai University, Faculty of Pharmacy,
  • Kindai University, Graduate School of Pharmacy,
  • Kinki University, Graduate School, Division of Pharmaceutical Sciences,

Research Activities

Research Areas

  • Life sciences, Pharmacology
  • Life sciences, Pharmaceuticals - health and biochemistry

Published Papers

  1. Sodium influx through cerebral sodium-glucose transporter type 1 exacerbates the development of cerebral ischemic neuronal damage
    Yui Yamazaki; Shinichi Harada; Tetsuyuki Wada; Teruki Hagiwara; Shigeru Yoshida; Shogo Tokuyama
    EUROPEAN JOURNAL OF PHARMACOLOGY  799  , 103-110, Mar. 2017  , Refereed
  2. Sodium transport through the cerebral sodium-glucose transporter exacerbates neuron damage during cerebral ischaemia
    Yui Yamazaki; Shinichi Harada; Tetsuyuki Wada; Shigeru Yoshida; Shogo Tokuyama
    JOURNAL OF PHARMACY AND PHARMACOLOGY  68  (7)  , 922-931, Jul. 2016  , Refereed
  3. Ouabain exerts cytoprotection by diminishing the intracellular K+ concentration increase caused by distinct stimuli in human leukemic cells
    Masayuki Takechi; Tetsuyuki Wada; Hideki Yagi; Takashi Masuko; Atsufumi Kawabata
    JOURNAL OF PHARMACY AND PHARMACOLOGY  67  (1)  , 126-132, Jan. 2015  , Refereed


Books etc

  1. ミネルヴァ書房, 『ケアマネジメント用語辞典(改訂版)』 , 南 武志; 吉田 繁; 巽 純子; 辻内 俊文; 和田 哲幸; 今西 孝至 , 2007
  2. ミネルヴァ書房, 『ケアマネジメント用語辞典』 , 南 武志; 吉田 繁; 巽 純子; 辻内 俊文; 和田 哲幸; 今西 孝至 , 2005

Conference Activities & Talks

  1. 医薬品の適正使用に関わる薬剤師の責務 ~薬学部教員からの視点~ , 和田哲幸; 片岡大士; 伊内秋夫; 志熊理史; 伊内 智; 秋本義雄 , 第60回 日本薬学会・日本薬剤師会・日本病院薬剤師会 中国四国支部学術大会 , Oct. 2021
  2. GPR120を介した性腺刺激ホルモン合成および分泌調節メカニズムについて , 森山隆太郎; 池田隼也; 原尚輝; 萩原央記; 和田哲幸 , 第114回日本繁殖生物学会大会 , Sep. 2021
  3. 患者のための医療サービスと薬局薬剤師業務負担に関する予備的意識調査 , 和田哲幸; 片岡大士; 瀧一洋; 米島貴夢; 伊内智; 伊内秋夫 , 第54回日本薬剤師会学術大会(福岡) , Sep. 2021



  1. Inhibitory effects of tetrahydroisoquinoline derivatives on Ca2+ and Na+ channels in crude nerve endings , Y Zhang; J Abe; T Wada; S Ichida; GY Xu , BIOLOGICAL & PHARMACEUTICAL BULLETIN , 23 , 3 , 375 , 378 , Mar. 2000
    Summary:Semi-synthetic tetrahydroisoquinoline derivatives prepared from natural alkaloids, possess Ca2+ antagonistic properties. These derivatives significantly blocked KCl-stimulated Ca2+ uptake (In chick and rat crude nerve endings) which fan be partially inhibited by the selective N-type Ca2+ channel blocker omega-conotoxin GVIA or the selective P-type Ca2+ channel blocker omega-agatoxin IVA. Moreover, PX42 (10 mu M; for the tetrahydroisoquinoline compounds in this study) could inhibit the activity of calmodulin-dependent phosphodiesterase and block veratridine-induced (or tetrodotoxin-sensitive) Na+ uptake. The possible mechanism(s) of non-selective inhibition of ion channels of PX42 is discussed.
  2. Calcium/calmodulin inhibits the binding of specific [I-125]omega-conotoxin GVIA to chick brain membranes , S Ichida; J Abe; YA Zhang; K Sugihara; K Imoto; T Wada; H Sohma , NEUROCHEMICAL RESEARCH , 25 , 3 , 335 , 340 , Mar. 2000
    Summary:The effect of Ca2+/calmodulin (CaM) on the specific binding of [I-125]omega-conotoxin GVIA (I-125-omega-CTX) to crude membranes from chick brain was investigated. When we examined the effects of the activation of various endogenous protein kinases on specific [I-125]omega-CTX binding to crude membranes, we observed that Ca2+/CaM had an inhibitory effect regardless of whether or not the standard medium contained ATP (0.5 mM). Ca2+/CaM also had an inhibitory effect in a simple binding-assay medium containing HEPES-HCl buffer, BSA, Ca2+ and CaM,and this effect was dependent on the concentration of Ca2+. The effect of Ca2+/CaM was attenuated by the CaM antagonists W-7 and CaM-kinase II fragment (290-309). An experiment with modified ELISA using purified anti omega-CTX antibody indicated that Ca2+/CaM did not affect the direct binding of [I-125]omega-CTX and CaM. These results suggest that Ca2+/CaM either directly or indirectly affects specific [I-125]omega-CTX binding sites, probably N-type Ca2+ channels in crude membranes from chick whole brain.
  3. Proportions of Ca2+ channel subtypes in chick or rat P2 fraction and NG108-15 cells using various Ca2+ blockers , Zhang Yu-an; Takashi Imanishi; Tetsuyuki Wada; Seiji Ichida , Neurochemical Research , 24 , 8 , 1059 , 1066 , 1999
    Summary:The proportions of calcium (Ca2+) channel subtypes in chick or rat P2 fraction and NG 108-15 cells were investigated using selective L-, N-, P- and P/Q- type Ca2+ channel blockers. KCl-stimulated 45Ca2+ uptake by chick P2 fraction was blocked by 40~50% using N-type Ca2+ channel blockers [ω- conotoxin GVIA, aminoglycoside antibiotics and dynorphin A(1-13)], but was not inhibited by P- or P/Q-type blockers (ω-agatoxin IVA or ω-conotoxin MVIIC). On the other hand, KCl-stimulated 45Ca2+ uptake by rat P2 fraction was blocked by 30~40% using P- or P/Q-type Ca2+ channel blockers, but was not inhibited by N-type Ca2+ channel blockers. The L-type Ca2+ channel blockers 1,4-dihydropyridines, diltiazem and verapamil, but not calciseptine (CaS), inhibited both KCl-stimulated 45Ca2+ uptake and veratridine-induced 22Na+ uptake by chick or rat P2 fraction with similar IC50 values. CaS did not have any effect on 45Ca2+ uptake by either chick or rat P2 fraction. In NG 108-15 cells, CaS, ω-agatoxin IVA and ω- conotoxin MVIIC, but not ω-conotoxin GVIA, inhibited KCl-stimulated 45Ca2+ uptake by 30-40%. Various combinations of these Ca2+ channel blockers had no significant additional effects in chick or rat P2 fraction or NG 108-15 cells. These findings suggest that KCl-stimulated 45Ca2+ uptake by chick or rat P2 fraction and NG 108-15 cells is a convenient and useful model for screening whether or not natural or synthetic substances have selective effects as L-, N-, P-, or P/Q- type Ca2+ channel antagonists or agonists.

Research Grants & Projects

  1. Study on characteristics of Specific 125I-ω-conotoxin GVTA binding sites
  2. 漏洩カリウムチャネルを標的とするウワバインの細胞保護機構解明