Endogenous nitric oxide inhibits bronchoconstriction induced by cold-air inhalation in guinea pigs: role of kinins.
Endogenous nitric oxide inhibits bronchoconstriction induced by cold-air inhalation in guinea pigs: role of kinins.
复制标题
内源性一氧化氮抑制豚鼠吸入冷空气引起的支气管收缩：激肽的作用。
DOI：
10.1164/ajrccm.157.2.9704074
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Geppetti,P
中科院分区：
文献类型：
--
作者：
Yoshihara,S;Nadel,JA;Figini,M;Emanueli,C;Pradelles,P;Geppetti,P
豚鼠吸入冷空气会增加总肺阻力（Rl），这种效应是由激肽和速激肽介导的。豚鼠吸入缓激肽（BK）引起的支气管收缩可被气道上皮一氧化氮（NO）释放明显抑制。我们研究了内源性NO是否调节吸入冷空气引起的r5的增加。在经阿托品预处理的麻醉和人工通气豚鼠中，吸入冷空气（气管内13°C） 5分钟不增加Rl。静脉注射ng -硝基-l-精氨酸甲酯（l-NAME）预处理（但不含其非活性对映体d-NAME）可增加Rl，这一作用被l-精氨酸逆转。速动素nk2受体拮抗剂SR 48968或速动素b2受体拮抗剂HOE 140可消除l- name后冷空气引起的r0升高。在给予sr48968后，吸入冷空气降低了基线气道张力。然而，在ho140后，冷空气吸入不影响基线气道张力。l-NAME可增强BK诱导的支气管收缩，而l-NAME对辣椒素诱导的支气管收缩无影响。BK增加体外豚鼠气管肌条中环鸟苷单磷酸（cGMP）水平，而选择性速激肽nk2受体激动剂[β Ala8]神经激肽A没有作用。目前的数据表明，冷空气吸入引起的支气管收缩和激肽和速激肽释放介导的支气管收缩被内源性NO抑制，激肽而不是速激肽或冷空气单独释放支气管松弛剂NO。
Inhalation of cold air in guinea pigs increases total pulmonary resistance (Rl), an effect that is mediated by kinins and tachykinins. Bronchoconstriction induced by bradykinin (BK) inhalation in guinea pigs is markedly inhibited by nitric oxide (NO) release from the airway epithelium. We investigated whether endogenous NO modulates the increase in Rlinduced by inhalation of cold air. In anesthetized and artificially ventilated guinea pigs pretreated with atropine, cold-air inhalation (13 ° C in the trachea) for 5 min did not increase Rl. Pretreatment with intravenous NG-nitro-l-arginine methyl ester (l-NAME) (but not with its inactive enantiomer,d-NAME) increased Rl, an effect reversed byl-Arg. The increase in Rlinduced by cold air afterl-NAME was abolished by the tachykinin NK2-receptor antagonist SR 48968 or the kinin B2-receptor antagonist, HOE 140. After administration of SR 48968, inhalation of cold air reduced baseline airway tone. However, after HOE 140, cold-air inhalation did not affect baseline airway tone.l-NAME exaggerated the bronchoconstriction induced by BK. However,l-NAME did not affect capsaicin-induced bronchoconstriction. BK increased cyclic guanosine monophosphate (cGMP) levels in strips of guinea pig trachealis musclein vitro, whereas the selective tachykinin NK2-receptor agonist [ β Ala8]neurokinin A was without effect. The present data suggest that bronchoconstriction induced by cold-air inhalation and mediated by kinin and tachykinin release is inhibited by endogenous NO, and that kinins, but not tachykinins or cold air alone, release bronchorelaxant NO.