Meyers K M, Huston L Y, Clemmons R M
Am J Physiol. 1983 Jul;245(1):R100-9. doi: 10.1152/ajpregu.1983.245.1.R100.
The action of epinephrine (E) on canine platelet aggregation is described. Although E did not induce a change in platelet shape or aggregation, potentiation of aggregation induced by the following agents was observed at physiological E concentrations (that is, less than 10 nM/1): arachidonic acid; the dense granule agonists, ADP and serotonin (5-HT); and collagen. Epinephrine-induced potentiation was in part independent of formation of arachidonic acid metabolites, and E potentiated the aggregating action of the bivalent cationophore A23187. Potentiation was inhibited by alpha-adrenergic receptor antagonists phenoxybenzamine, phentolamine, and ergotamine, and mimicked by alpha-adrenergic receptor agonists norepinephrine, clonidine, and in some cases, phenylephrine. The beta-adrenergic receptor agonists isoproterenol and dobutamine inhibited ADP-induced aggregation, and this action was presented by pretreating the platelets with propranolol and dichloroisoproterenol. An augmentation of the aggregation response of platelets to arachidonic acid was observed in blood samples withdrawn when circulating catecholamines were elevated. The physiological implication of epinephrine acting as a gain controller that alters the relationship between actuating signal and the platelet response to an agonist is discussed.
本文描述了肾上腺素（E）对犬血小板聚集的作用。尽管E不会引起血小板形状或聚集的改变，但在生理浓度的E（即小于10 nM/1）下，可观察到它对以下试剂诱导的聚集有增强作用：花生四烯酸；致密颗粒激动剂、二磷酸腺苷（ADP）和5-羟色胺（5-HT）；以及胶原蛋白。肾上腺素诱导的增强作用部分独立于花生四烯酸代谢产物的形成，并且E增强了二价阳离子载体A23187的聚集作用。α-肾上腺素能受体拮抗剂酚苄明、酚妥拉明和麦角胺可抑制这种增强作用，而α-肾上腺素能受体激动剂去甲肾上腺素、可乐定以及在某些情况下的去氧肾上腺素可模拟这种增强作用。β-肾上腺素能受体激动剂异丙肾上腺素和多巴酚丁胺可抑制ADP诱导的聚集，并且用普萘洛尔和二氯异丙肾上腺素预处理血小板可呈现这种作用。在循环儿茶酚胺升高时采集的血样中，观察到血小板对花生四烯酸的聚集反应增强。本文讨论了肾上腺素作为增益控制器改变启动信号与血小板对激动剂反应之间关系的生理意义。
