Nagano Y, Tamaoki J, Nishimura K, Yamawaki I, Nagai A
First Department of Medicine, Tokyo Women's Medical University School of Medicine, Japan.
Res Commun Mol Pathol Pharmacol. 2000 Jul-Aug;108(1-2):96-107.
To determine whether adenosine A3 receptor stimulation produces airway inflammation and, if so, what the mechanism of action is, we studied microvascular permeability in the rat trachea. After intravenous injection of Evans blue dye, adenosine and various adenosine analogues were given by inhalation, and the tracheal microvascular permeability was determined by a photometric measurement of extravasated dye. N6-2-(4-aminophenyl)-ethyladenosine (APNEA), an adenosine A3 receptor agonist, dose dependently increased plasma protein extravasation, whereas adenosine, the A1-receptor agonist N6-(R-phenylisopropyl)-adenosine, or the A2-receptor agonist 5'-N-ethyl-carboxamidoadenosine had no effect. The effect of APNEA was not altered by the adenosine A1/A2 receptor antagonist 8-(p-sulphophenyl)-theophylline, but was reduced by depletion of mast cell-derived mediators with compound 48/80 or pretreatment with the tachykinin NK1 receptor antagonist CP99,994. These results suggest that activation of A3 receptor specifically increase airway microvascular permeability probably via mast cell-derived mediators and tachykinins.
为了确定腺苷A3受体刺激是否会引起气道炎症，以及如果会引起炎症，其作用机制是什么，我们研究了大鼠气管中的微血管通透性。静脉注射伊文思蓝染料后，通过吸入给予腺苷和各种腺苷类似物，并通过对渗出染料的光度测量来测定气管微血管通透性。腺苷A3受体激动剂N6-2-(4-氨基苯基)-乙基腺苷(APNEA)剂量依赖性地增加血浆蛋白外渗，而腺苷、A1受体激动剂N6-(R-苯异丙基)-腺苷或A2受体激动剂5'-N-乙基-羧酰胺腺苷则无此作用。腺苷A1/A2受体拮抗剂8-(对-磺基苯基)-茶碱不会改变APNEA的作用，但用化合物48/80耗尽肥大细胞衍生介质或用速激肽NK1受体拮抗剂CP99,994预处理会降低APNEA的作用。这些结果表明，A3受体的激活可能通过肥大细胞衍生介质和速激肽特异性增加气道微血管通透性。
