Susanna V, Loffreda A, Matera M G, Servodio R, Filippelli A, Santagata A, Montanaro C, Carapella N, Marmo E
Department of Pharmacology and Toxicology, 1st Faculty of Medicine and Surgery, University of Naples, Italy.
Int J Tissue React. 1990;12(1):59-65.
We have investigated the effect of inhaled adenosine on bronchomotor tone in 16 healthy and 24 allergic and non-allergic bronchopathic subjects. We determined the inhaled adenosine dose-response curves after no treatment and after treatment with aminophylline (240 mg in 10 min), reproterol (90 mcg in 2 min) and salbutamol (100 mcg in 2 min) administered intravenously 15 min before adenosine and reproterol (500 mcg) and salbutamol (200 mcg) administered by inhalation from a metered aerosol 30 min before adenosine on separate days. Without prior treatment, inhaled adenosine caused bronchoconstriction in both groups of subjects (normal, and atopic and non-atopic asthmatic ones), but the peripheral airways revealed only a moderate change in normal subjects. Aminophylline caused a greater inhibition of adenosine bronchoconstriction than did reproterol. These results suggest that inhaled adenosine bronchoconstriction involved purinergic transmission and that it is mediated via a P1/Ri (A-1/R1) receptor. Aminophylline is a potent antagonist at purinoceptor level. Reproterol inhibits bronchoconstriction by a mechanism independent of its effect on beta-adrenergic receptors. Because salbutamol, i.e. a beta 2-agonist bronchodilator, did not inhibit adenosine-induced bronchoconstriction (or very nearly so), our results support the view that reproterol antagonizes P1/Ri (A1/R1) tracheobronchial receptors.
我们研究了吸入腺苷对16名健康受试者以及24名变应性和非变应性支气管病患者支气管运动张力的影响。我们分别测定了未经治疗以及在腺苷吸入前15分钟静脉注射氨茶碱（10分钟内注射240毫克）、瑞普特罗（2分钟内注射90微克）和沙丁胺醇（2分钟内注射100微克），以及在腺苷吸入前30分钟通过定量气雾剂吸入瑞普特罗（500微克）和沙丁胺醇（200微克）后的吸入腺苷剂量反应曲线。未经预先治疗时，吸入腺苷在两组受试者（正常受试者以及特应性和非特应性哮喘患者）中均引起支气管收缩，但外周气道在正常受试者中仅显示出中度变化。氨茶碱对腺苷支气管收缩的抑制作用比利丙喘定更强。这些结果表明，吸入腺苷引起的支气管收缩涉及嘌呤能传递，且是通过P1/Ri（A-1/R1）受体介导的。氨茶碱在嘌呤受体水平是一种强效拮抗剂。瑞普特罗通过一种独立于其对β-肾上腺素能受体作用的机制抑制支气管收缩。由于β2-激动剂支气管扩张剂沙丁胺醇并未抑制腺苷诱导的支气管收缩（或几乎未抑制），我们的结果支持瑞普特罗拮抗P1/Ri（A1/R1）气管支气管受体这一观点。
