Ding Y A, MacIntyre D E, Kenyon C J, Semple P F
MRC Blood Pressure Unit, Western Infirmary, Glasgow, Scotland.
J Hypertens Suppl. 1985 Dec;3(3):S251-3.
The effects of angiotensin II (ANG II) alone and in combination with other agonists on platelet aggregation, thromboxane B2 (TxB2) synthesis and cytosolic [Ca2+]i were investigated. Angiotensin II (10(-11)-10(-7) mol/l) alone had no direct effect on aggregation, TxB2 production or [Ca2+]i after short- (< 2 min) or long-term (30 min) incubation. In contrast, low concentrations of ANG II (10(-11) mol/l) enhanced adrenaline-induced platelet aggregation but high concentrations (10(-7) mol/l) had an inhibitory effect. Moreover, ANG II (10(-11)-10(-7) mol/l) augmented platelet responses to the TxA2 mimetic U44069. The facilitatory effect of ANG II on adrenaline-induced platelet aggregation was abolished by pretreatment of platelets with flurbiprofen. Thromboxane B2 synthesis by adrenaline-treated platelets was inhibited by ANG II. The results indicate that ANG II stimulation of agonist-induced platelet activation is due to potentiation of the effects rather than the synthesis of TxA2.
研究了单独使用血管紧张素 II（ANG II）以及与其他激动剂联合使用对血小板聚集、血栓素 B2（TxB2）合成和细胞内钙离子浓度（[Ca2+]i）的影响。单独使用血管紧张素 II（10^(-11) - 10^(-7) mol/L），在短期（<2 分钟）或长期（30 分钟）孵育后，对聚集、TxB2 生成或[Ca2+]i 均无直接影响。相比之下，低浓度的 ANG II（10^(-11) mol/L）增强了肾上腺素诱导的血小板聚集，而高浓度（10^(-7) mol/L）则具有抑制作用。此外，ANG II（10^(-11) - 10^(-7) mol/L）增强了血小板对 TxA2 模拟物 U44069 的反应。用氟比洛芬预处理血小板可消除 ANG II 对肾上腺素诱导的血小板聚集的促进作用。ANG II 抑制了肾上腺素处理的血小板的 TxB2 合成。结果表明，ANG II 对激动剂诱导的血小板活化的刺激作用是由于效应的增强而非 TxA2 的合成。
