Adenosine inhibits leukocyte-induced vasoconstriction.
Adenosine inhibits leukocyte-induced vasoconstriction.
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腺苷抑制白细胞诱导的血管收缩。
DOI：
10.1152/ajpheart.1996.271.6.h2622
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
T. Kamada
中科院分区：
文献类型：
--
作者：
T. Minamino;M. Kitakaze;K. Node;H. Funaya;M. Inoue;M. Hori;T. Kamada
多形核白细胞（PMN）可以诱导内皮依赖性血管环收缩。由于腺苷抑制中性粒细胞的功能，我们研究了腺苷对中性粒细胞诱导的冠状血管收缩的影响。在添加自体 PMN 后，我们测量了悬浮在充满 Krebs-Henseleit 溶液的器官室中的犬冠状动脉孤立环的等长张力变化。 N-甲酰-L-甲硫氨酰-亮氨酰-苯丙氨酸 (FMLP) 刺激的 PMN 以浓度依赖性方式增加冠状动脉与内皮的张力。用腺苷处理 FMLP 刺激的 PMN 既抑制了 PMN 与内皮的粘附，也抑制了 PMN 诱导的血管收缩。用 CGS-21680C（而非环己基腺苷）刺激 PMN，可以抑制 PMN 与内皮的粘附以及 PMN 诱导的血管收缩。然而，用腺苷治疗冠状动脉对中性粒细胞与内皮的粘附以及中性粒细胞引起的收缩没有影响。这些结果表明，刺激 PMN 上的腺苷 A2a 受体可能通过抑制 PMN 与内皮的粘附来抑制 PMN 诱导的血管收缩。
Polymorphonuclear leukocytes (PMNs) can induce endothelium-dependent constriction of vascular rings. Because adenosine inhibits the function of PMNs, we examined the effects of adenosine on the PMN-induced coronary vasoconstriction. We measured changes in the isometric tension of isolated rings of canine coronary arteries suspended in an organ chamber filled with Krebs-Henseleit solution after the addition of autologous PMNs. N-formyl-L-methionyl-leucyl-phenylalanine (FMLP)-stimulated PMNs increased the tension of the coronary artery with the endothelium in a concentration-dependent manner. Treatment of FMLP-stimulated PMNs with adenosine inhibited both the adhesion of PMNs to the endothelium and the PMN-induced vasoconstriction. Stimulation of PMNs with CGS-21680C, but not with cyclohexyladenosine, inhibited both the adhesion of PMNs to the endothelium and the PMN-induced vasoconstriction. However, treatment of coronary arteries with adenosine had no effect on the adherence of PMNs to the endothelium and the PMN-induced constriction. These results suggest that stimulation of adenosine A2a receptors on PMNs may inhibit the PMN-induced vasoconstriction by inhibiting the adhesion of PMNs to the endothelium.