Tamaoki J, Chiyotani A, Kondo M, Konno K
First Department of Medicine, Tokyo Women's Medical College, Japan.
Am J Physiol. 1995 Jun;268(6 Pt 1):C1342-7. doi: 10.1152/ajpcell.1995.268.6.C1342.
To determine possible contribution of nitric oxide (NO) to the stimulatory action of beta-adrenoceptor agonist on ciliary motility, we measured ciliary beat frequency (CBF) of rabbit cultured tracheal epithelial cells by photoelectric method and NO release by specific amperometric sensors for this molecule in vitro. Salbutamol increased CBF, an effect that was potentiated by superoxide dismutase. Pretreatment of cells with NG-nitro-L-arginine methyl ester (L-NAME) attenuated the salbutamol-induced increase in CBF, causing a rightward displacement of the concentration-response curve by 2-2.5 log units, whereas NG-nitro-D-arginine methyl ester had no effect. The inhibitory effect of L-NAME was reversed by L-arginine but not by D-arginine. Immersion of the NO-selective electrode in the medium containing epithelial cells detected baseline current of 4.6-14.5 pA, which was abolished by L-NAME. Salbutamol dose-dependently increased the concentration of NO in the medium, the maximal increase being 56.2 +/- 5.3 nM (mean +/- SE; P < 0.001). These results suggest that NO is spontaneously released by airway epithelium and that the enhanced release of this molecule may play a role in the beta-adrenoceptor-mediated stimulation of ciliary motility.
为了确定一氧化氮（NO）对β-肾上腺素能受体激动剂刺激纤毛运动作用的可能贡献，我们采用光电方法测量了兔培养气管上皮细胞的纤毛搏动频率（CBF），并在体外使用针对该分子的特异性电流传感器测量了NO释放。沙丁胺醇增加了CBF，超氧化物歧化酶可增强这一作用。用NG-硝基-L-精氨酸甲酯（L-NAME）预处理细胞可减弱沙丁胺醇诱导的CBF增加，使浓度-反应曲线向右移位2-2.5个对数单位，而NG-硝基-D-精氨酸甲酯则无作用。L-NAME的抑制作用可被L-精氨酸逆转，但不能被D-精氨酸逆转。将NO选择性电极浸入含有上皮细胞的培养基中可检测到4.6-14.5 pA的基线电流，该电流可被L-NAME消除。沙丁胺醇剂量依赖性地增加培养基中NO的浓度，最大增加量为56.2±5.3 nM（平均值±标准误；P<0.001）。这些结果表明，气道上皮细胞可自发释放NO，且该分子释放的增强可能在β-肾上腺素能受体介导的纤毛运动刺激中起作用。
