In order to examine the role of nitric oxide (NO) on airway mucus secretion we studied the effects of the nitric oxide synthase (NOS) inhibitor L-N(G)-monomethyl-L-arginine (L-NMMA), a novel nitric oxide donor, (+/-)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexeneamide (FK409), and the NO precursor L-arginine on basal mucus secretion in the ferret trachea in vitro in Ussing chambers. We also determined the effects of these agents upon secretion induced by electrical stimulation of nerves or by acetylcholine (ACh). We used 35SO4 as a mucus marker. 2. L-NMMA (0.01-1 mM) increased basal output of 35SO4-labelled macromolecules with a maximal increase above baseline of 248% at 0.1 mM L-NMMA. L-Arginine (1 mM) alone had no significant effect on basal secretion but reversed the potentiating effect of L-NMMA on basal secretion. L-NMMA-induced increases in basal mucus secretion were sustained for at least 30 min in the continuing presence of the NOS inhibitor. In contrast to the potentiating effects of L-NMMA, FK409 (100 nM) reduced basal secretion by 60% (at 1 nM and at 10 nM it was without effect). 3. Electrical stimulation (50 V, 10 Hz, 0.5 ms for 5 min) increased 35SO4 output by 174%. L-NMMA (1 and 10 mM) present during stimulation of tracheal segments resulted in significant potentiations of 214% and 116%, respectively, of the neurogenic response. The potentiated response to 10 mM L-NMMA was reversed by L-arginine (1 mM). At this dose L-arginine had no effect itself on basal secretion. In contrast to the potentiating effects of L-NMMA on neurogenic secretion, FK409 at 10 nM and 100 nM inhibited the neurogenic response by 98% and 99%. 4. At all concentrations tested, neither L-NMMA (0.01 mM-1 mM) nor FK409 (1-100 mM) had any significant effect on ACh-induced mucus secretion. 5. These observations lead us to conclude that nitric oxide, derived from constitutive NO synthase, acts as an endogenous inhibitor of both basal and neurogenic mucus secretion in ferret trachea in vitro.
摘要
为了研究一氧化氮(NO)对气道黏液分泌的作用,我们在尤斯灌流小室中体外研究了一氧化氮合酶(NOS)抑制剂L-N(G)-单甲基-L-精氨酸(L-NMMA)、一种新型一氧化氮供体(+/-)-(E)-乙基-2-[(E)-羟基亚氨基]-5-硝基-3-己烯酰胺(FK409)以及NO前体L-精氨酸对雪貂气管基础黏液分泌的影响。我们还测定了这些药物对神经电刺激或乙酰胆碱(ACh)诱导的分泌的影响。我们使用35SO4作为黏液标记物。2. L-NMMA(0.01 - 1 mM)增加了35SO4标记的大分子的基础分泌量,在0.1 mM L-NMMA时,比基线的最大增加量为248%。单独的L-精氨酸(1 mM)对基础分泌没有显著影响,但可逆转L-NMMA对基础分泌的增强作用。在持续存在NOS抑制剂的情况下,L-NMMA诱导的基础黏液分泌增加持续至少30分钟。与L-NMMA的增强作用相反,FK409(100 nM)使基础分泌减少了60%(在1 nM和10 nM时无作用)。3. 电刺激(50 V,10 Hz,0.5 ms,持续5分钟)使35SO4分泌量增加了174%。在气管段刺激期间存在的L-NMMA(1和10 mM)分别使神经源性反应显著增强了214%和116%。L-精氨酸(1 mM)逆转了对10 mM L-NMMA的增强反应。在此剂量下,L-精氨酸本身对基础分泌没有影响。与L-NMMA对神经源性分泌的增强作用相反,10 nM和100 nM的FK409分别抑制神经源性反应98%和99%。4. 在所有测试浓度下,L-NMMA(0.01 mM - 1 mM)和FK409(1 - 100 mM)对ACh诱导的黏液分泌均无显著影响。5. 这些观察结果使我们得出结论,由组成型NO合酶产生的一氧化氮在体外作为雪貂气管基础和神经源性黏液分泌的内源性抑制剂。