Takemura H, Tamaoki J, Tagaya E, Chiyotani A, Kondo M, Konno K
First Department of Medicine, Tokyo Women's Medical College.
Arerugi. 1995 Apr;44(4):474-80.
To examine the effect of tachykinins on Cl secretion across tracheal mucosa and the possible contribution of nitric oxide (NO) formation to their actions in vivo, we measured Cl diffusion potential difference (Cl-PD) with a high-impedance voltmeter in the presence of amiloride. Superfusion of each neurokinin A (NKA) and substance P (SP) increased Cl-PD in a concentration-dependent fashion, whereas neurokinin B (NKB) had no effect, with the rank order of potency being NKA > SP >> NKB. The tachykinin-induced increase in Cl-PD was inhibited by the NO synthase inhibitor NG-nitro-L-arginine methylester (L-NAME), an effect that was reversed by L-arginine but not by D-arginine. These results suggest that tachykinins increase Cl secretion across rabbit trachea from the submucosa toward the lumen via stimulation of NK2 receptors and that NO formation may be involved in at least part of this process.
为了研究速激肽对气管黏膜氯分泌的影响以及一氧化氮（NO）生成在其体内作用中的可能贡献，我们在存在氨氯吡咪的情况下，用高阻抗电压表测量了氯扩散电位差（Cl-PD）。每种神经激肽A（NKA）和P物质（SP）的灌流均以浓度依赖的方式增加了Cl-PD，而神经激肽B（NKB）则无作用，其效力顺序为NKA > SP >> NKB。速激肽诱导的Cl-PD增加被NO合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）抑制，L-精氨酸可逆转此效应，而D-精氨酸则不能。这些结果表明，速激肽通过刺激NK2受体增加兔气管从黏膜下层向管腔的氯分泌，并且NO生成可能至少部分参与了这一过程。
