Negresku E V, Baldenkov G N, Grigorian G Iu, Mazaev A V, Tkachuk V A
Biokhimiia. 1989 Jun;54(6):909-15.
Epinephrine (E) and norepinephrine (NE) alone did not increase free intracellular Ca2+ ([Ca2+]i) in human platelets loaded with Quin-2 or Fura-2; however, they did potentiate the effects of vasopressin (VP), serotonin (S) and platelet activating factor (PAF). The synergism in [Ca2+]i increase was also obtained in the presence of VP together with PAF, S with PAF as well as VP with S. The effect of E or NE was blocked by yohimbine and phentolamine. Prazosin was less effective, while propranolol had no effect at all. Clonidine did not potentiate the effects of VP, S or PAF on [Ca2+]i; however, it did block the potentiation induced by E or NE. E potentiated the VP-induced 45Ca2+ uptake as well as VP-stimulated inositol 1,4,5-trisphosphate (IP3) formation. E alone did not change significantly the level of IP3 in platelets, nor did it influence the cyclic AMP level. The experimental results suggest that both Ca2+ influx and polyphosphoinositide breakdown underlie the mechanism of potentiation.
单独使用肾上腺素（E）和去甲肾上腺素（NE）不会增加负载喹啉-2或氟罗红-2的人血小板中的游离细胞内钙离子浓度（[Ca2+]i）；然而，它们确实能增强血管加压素（VP）、5-羟色胺（S）和血小板活化因子（PAF）的作用。在VP与PAF、S与PAF以及VP与S共同存在的情况下，也能观察到[Ca2+]i增加的协同作用。E或NE的作用可被育亨宾和酚妥拉明阻断。哌唑嗪的效果较差，而普萘洛尔则完全没有作用。可乐定不会增强VP、S或PAF对[Ca2+]i的作用；然而，它确实能阻断E或NE诱导的增强作用。E增强了VP诱导的45Ca2+摄取以及VP刺激的肌醇1,4,5-三磷酸（IP3）的形成。单独使用E不会显著改变血小板中IP3的水平，也不会影响环磷酸腺苷水平。实验结果表明，钙离子内流和多磷酸肌醇分解均是增强作用机制的基础。
