THROMBOXANE-A2 PROSTAGLANDIN-H2 MOBILIZES CALCIUM IN HUMAN-BLOOD PLATELETS
THROMBOXANE-A2 PROSTAGLANDIN-H2 MOBILIZES CALCIUM IN HUMAN-BLOOD PLATELETS
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DOI：
10.1152/ajpheart.1985.249.1.h1
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发表时间：
1985-01-01
影响因子：
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通讯作者：
LEBRETON, GC
中科院分区：
文献类型：
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作者：
BRACE, LD;VENTON, DL;LEBRETON, GC
探讨血栓素A2/前列腺素H2 （TXA2/PGH2）刺激血小板活化的机制。显然，TXA2/PGH2的功能是释放血小板内储存的钙。研究了TXA2/PGH2是否引起完整血小板中Ca的动员。使用荧光探针、氯四环素（CTC）和光子计数显微荧光仪测量钙的再分布。人富血小板血浆用CTC （50 .mu）孵育。温度25度，40分钟。C.花生四烯酸（AA, 100 .mu）诱导植株形状改变。M)或ADP （0.75-1.0 . μ M）。AA的加入导致血小板内钙的显著释放，这种释放被吲哚美辛（20.mu）抑制环加氧酶所阻断。M)或特定的TXA2/PGH2拮抗剂13-氮杂腺苷酸（13-APA, 100 μ M）。吲哚美辛和13-APA对ADP刺激的Ca释放均无影响。前列环素（13 nM）对AA-和adp诱导的Ca释放均有抑制作用。这些发现证明，AA的环加氧酶产物，即TXA2和/或PGH2，直接引起血小板内Ca的动员。这种Ca的动员似乎是通过特定的TXA2/PGH2受体相互作用介导的。
The mechanism by which thromboxane A2/prostaglandin H2 (TXA2/PGH2) stimulates platelet activation was investigated. Apparently TXA2/PGH2 functions to release Ca from intraplatelet stores. It was investigated whether TXA2/PGH2 causes mobilization of Ca in intact platelets. Ca redistribution was measured using the fluorescent probe, chlortetracycline (CTC), and a photon-counting microspectrofluorometer. Human platelet-rich plasma was incubated with CTC (50 .mu.M) for 40 min at 25.degree. C. Shape change was induced with arachidonic acid (AA, 100 .mu.M) or ADP (0.75-1.0 .mu.M). AA addition resulted in a significant release of intraplatelet Ca. This release was blocked by inhibition of the cyclooxygenase with indomethacin (20 .mu.M) or the specific TXA2/PGH2 antagonist, 13-azaprostanoic acid (13-APA, 100 .mu.M). Neither indomethacin nor 13-APA had any effect on Ca release stimulated by ADP. Prostacyclin (13 nM) inhibited both AA- and ADP-induced Ca release. These findings provide evidence that cyclooxygenase products of AA, i.e., TXA2 and/or PGH2, directly caused the mobilization of intraplatelet Ca. This Ca mobilization appears to be mediated through a specific TXA2/PGH2 receptor interaction.