Kenzo Kikuchi
Takeda Pharmaceutical Company
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Featured researches published by Kenzo Kikuchi.
Life Sciences | 1981
Go Kito; Hiroko Okuda; Shigenori Ohkawa; Shinji Terao; Kenzo Kikuchi
Abstract Leukotrienes C4 (LTC4) and D4 (LTD4), major components of slow-reacting substances of anaphylaxis (SRS-A), caused dose-dependent contractions of rabbit coronary arteries in concentrations of 10−9 to 10−7 M and 10−10 to 10−7 M, respectively. The potency of LTC4 and LTD4, when compared with the concentration that elicits half of the contraction induced by 25 mM KCl, was 17 and 76 times, respectively, greater than that of histamine. In contrast, other blood vessels from rabbits were either unresponsive (renal artery and vein, mesenteric artery and thoracic aorta) or only weakly responsive (pulmonary artery and vein and portal vein) to both leukotrienes even at 10−7 M. The LTD4-induced coronary contraction was inhibited by FPL 55712 (10−7 and 10−6 M), a selective SRS-A inhibitor, in a dose-dependent manner, but not by diphenhydramine (10−7 M), a histamine H1-receptor blocker or by indomethacin (10−5 M), a prostaglandin synthetase inhibitor, suggesting that LTD4 has a direct effect on the coronary arteries. These results indicate that the leukotrienes may act as potent, selective coronary vasoconstrictors and that SRS-A responsive receptors exist in the rabbit coronary artery.
Journal of Molecular and Cellular Cardiology | 1977
Kiyota Goshima; Takeshi Honda; Minoru Hirata; Kenzo Kikuchi; Yoshifumi Takeda; Toshio Miwatani
Abstract The effects of a highly purified toxin from Vibrio parahaemolyticus on the beating of cultured mouse and rat myocardial cells and isolated rat atrial preparations were examined. Low concentrations of the toxin stopped the beating of both single isolated myocardial cells and cell clusters obtained in culture from fetal mouse and fetal rat ventricles. These low concentrations depolarized the maximal diastolic potentials and inhibited the generation of action potentials of cultured myocardial cells. The beating activity and the normal generation of action potentials were regained on washing off the toxin or on incubating the cells further in the presence of the toxin. The toxin lost its ability to stop the beating when it was preincubated with the ganglioside, G T1 or G M1 . Spontaneous beating of isolated adult rat atrial preparations stopped in the diastolic phase on addition of the toxin. Before the beating stopped completely, temporary increase in the developed tension and irregular contractions were seen. High concentrations of the toxin caused morphological damage of cultured myocardial cells from fetal mouse and fetal rat ventricles, but did not stop the spontaneous beating, or cause morphological damage of cultured myocardial cells from embryonic chick ventricles.
Japanese Journal of Pharmacology | 1970
Kenzo Kikuchi; Minoru Hirata; Akinobu Nagaoka
Japanese Journal of Pharmacology | 1970
Kenzo Kikuchi; Minoru Hirata; Akinobu Nagaoka; Yoshitomo Aramaki
Japanese Journal of Pharmacology | 1970
Minoru Hirata; Kenzo Kikuchi
Japanese Journal of Pharmacology | 1969
Akinobu Nagaoka; Kenzo Kikuchi; Yoshitomo Aramaki
Japanese Circulation Journal-english Edition | 1970
Akinobu Nagaoka; Kenzo Kikuchi; Yoshitomo Aramaki
Japanese Circulation Journal-english Edition | 1971
Akinobu Nagaoka; Katsuichiro Sudo; Shigeru Orita; Kenzo Kikuchi; Yoshitomo Aramaki
Chemical & Pharmaceutical Bulletin | 1974
Takuichi Miki; Kentaro Hiraga; Hirotomo Masuya; Tsunehiko Asako; Shoichiro Fujii; Kiyohisa Kawai; Kenzo Kikuchi; Shigeru Shintani; Minoru Yamazaki
Japanese Circulation Journal-english Edition | 1970
Minoru Hirata; Kenzo Kikuchi; Koroku Hashimoto