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• W1983776278 abstract "It is generally accepted that intracellular Ca2+ is a key substance in the intracellular signal transducing mechanism of platelets. We investigated the possibility that extracellular and/or intracellular Ca2+ might regulate the transport activity of serotonin (5-HT) into platelets. We found thatextracellular Ca2+ chelation with EGTA caused inhibition of 5HT uptake activity, which was recovered by extracellulary applied excess Ca2+. Intracellular Ca2+ chelation with acetoxymethyl bis(O-aminophenoxy)ethane-N,N,N′,N′-tetraacetate (BAPTA-AM) did not, however, have any inhibitory effect on 5HT uptake activity in the presence of extracellular Ca2+. In the absence of extracellular Ca2+, BAPTA-AM significantly inhibited 5-HT uptake. The restorative effect of Ca2+ on 5-HT transport into EGTA-treated platelets was mimicked by Ba2+, but not by Sr2+. It was antagonised by inorganic Ca2+ channel antagonist including Ni2+, La3+ and Gd3+, but not by organic Ca2+ channel blockers including verapamil, nifedipine, diltiazem, ω-conotoxin GVIA and α-agatoxin IVA. Furthermore, 3,4,5-trimethoxybenzoic acid 8-(diethylamino)acytl ester hydrochloride (TMB-8), an intracellular Ca2+ antagonist, was found to inhibit the restorative effect of Ca2+. These results have led to the suggestion that depletion of intracellular Ca2+ pool(s) by EGTA might result in a reduction of 5-HT uptake activity. Thus, the intracellular Ca2+ pool(s) susceptible to EGTA might have a regulatory role in maintaining 5-HT transport into blood platelets." @default.
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• W1983776278 date "1995-01-01" @default.
• W1983776278 modified "2023-09-27" @default.
• W1983776278 title "Role of calcium ion in platelet serotonin uptake regulation" @default.
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• W1983776278 doi "https://doi.org/10.1016/0922-4106(95)90189-2" @default.
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