作者: Yasunobu SUKETA , Kenji SUZUKI , Toshinobu TAKI , Yasuko ITOH , Masaru YAMAGUCHI
DOI: 10.1248/BPB.18.273
关键词: Brush border 、 Sodium fluoride 、 Calphostin C 、 Cotransporter 、 Na+/K+-ATPase 、 Kidney 、 Internal medicine 、 Sodium 、 Endocrinology 、 Chemistry 、 Fluoride
摘要: In this study, renal Na+/K+-ATPase activity was demonstrated to be strongly suppressed prior the glucosuria caused by a fluoride dose (NaF 35mg/kg, i. p.), and 50% suppression of enzyme almost at same NaF, about 30mg/kg, i.p. rats. rats, Na+/glucose cotransporter in brush border membranes not affected vivo whereas basolateral showed dip 3h after NaF treatment whole animal. Moreover, it suggested from experiments with inhibitors calphostin C KT5720 that protein kinase C, but A, may play an important role following administration fairly insensitive being competitively inhibited Ki 100 mM, much more sensitive, 2 mM. From these results, elevation urinary glucose excretion single deduced due direct and/or secondary action fluoride, rather than corresponding activity.