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目的研究是否β肾上腺素能受体（β－受体）激动增加人血小板一氧化氮合酶（ＮＯＳ）活性。方法利用Ｓｅｐｈａｒｏｓｅ凝胶柱分高血小板，根据ＮＯＳ能转换Ｌ－精氨酸为Ｌ－瓜氨酸的原理，观察基础状态下，给予ＮＯＳ合酶阻滞剂、Ｌ－ＮＭＭＡ、激动剂组织胺和β受体激动剂异丙肾上腺素后ＮＯＳ活性变化，以及选择性β受体亚型阻断后对异而肾上腺素作用影响。结果基础状态下人类血小板有ＮＯ释放，Ｌ－ＮＭＭＡ能明显抑制这种释放，组胺和异丙肾上腺素均能明显增加血小板ＮＯＳ活性，β２受体阻断剂能完全阻断异丙肾上腺素增加 ＮＯＳ活性的作用。结论异丙肾上腺素能增加血小板ＮＯＳ活性，这种作用是通过β２受体介导。
Aim To investigate whether agonism of beta adrenergic receptors (beta-receptors) increases the activity of human platelet nitric oxide synthase (NOS). Methods According to the principle that NOS can convert L-arginine into L-citrulline by Sepharose gel column, the effect of NOS synthase blocker, L-NMMA, agonist histamine and The change of NOS activity after β-agonist isoproterenol and the effect of different-type epinephrine after blocking of selective β-receptor subtype. Results Under the basal conditions, NO was released from human platelets, and L-NMMA significantly inhibited this release. Histamine and isoproterenol significantly increased platelet NOS activity, while β2 receptor blockers completely blocked the increase of isoproterenol NOS activity. Conclusion Isoproterenol can increase platelet NOS activity, which is mediated by β2 receptors.