| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
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| Research Abstract |
The aim of this investigation was to clarify the mechanism of alkalization induced by neurotransmitters in human salivary gland. Cells of the HSG cell (a cell line from human submandibular adenocarcinoma) and A-431 cell (a human epidermoid carcinoma cell line) were loaded with a fluorescent pH indicator, BCECF/AM,and the change in the intracellular pH of them was measured following stimulation with various concentrations (10^<-7>M to 10^<-2>M) of neurotransmitters (carbachol, noradrenaline, and isoproterenol). Isoproterenol did not cause alkalization of either cell type at all, whereas, noradrenaline and carbachol alkalized both types over the concentration ranges of 10^<-6>M to 3*10^<-3>M (HSG cell by noradrenaline), 10^<-7>M to 2*10^<-4>M (A-431 cell by noradrenaline), and 7*10^<-5>M to 10^<-4>M (A-431 cell by carbacho1). On the other hand, alkalization induced by carbachol in the HSG cells was recognized at concentrations higher than 6*10^<-5>M,and it showed no upper limit in terms of carbachol concentration. This high-dose carbachol alkalization was not eliminated by preincubation with nifedipine (100 muM), Ca^<2+> channel blocker, or with thapsigargin (100 muM), amicrosomal Ca^<2+> -ATPase inhibitor. The alkalization system of HSG cell was quite different from that in the else epithelial cells and that induced by high-dose carbachol in the HSG cell appears to be independent of intracellular Ca^<2+>.
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