Pre- and postjunctional effects of a thromboxane mimetic in canine bronchi.
Pre- and postjunctional effects of a thromboxane mimetic in canine bronchi.
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血栓素模拟物在犬支气管中的交界前和交界后效应。
DOI：
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发表时间：
1991
影响因子：
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通讯作者：
E. Daniel
中科院分区：
文献类型：
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作者：
L. Janssen;E. Daniel
血栓素A2被认为参与引起气道平滑肌（ASM）的高反应性。因此，我们研究了血栓素模拟物（U-46619）对犬支气管ASM（第3至第5阶）的孤立环段的影响。发现U-46619（10（-9）-10（-5）M）引起强直性收缩、膜去极化和膜电位振荡。这些效应对血栓素受体的阻断敏感（使用10（-8）M L 670，596）;机械反应对3 × 10（-8）M阿托品、10（-7）M尼群地平或暴露于无Ca（2+）介质[（含有0.5 mM乙二醇-双（β-氨基乙基醚）-N，N，N '，N'-四乙酸（EGTA）]不敏感。U-46619还增强电场刺激引起的收缩和兴奋性连接电位，而不改变对卡巴胆碱的敏感性。这种增强作用对L 670，596也敏感，但对肾上腺素能受体的阻滞剂（使用酚妥拉明加普萘洛尔）不敏感。我们的结论是，犬支气管ASM具有连接前和连接后血栓素受体。前者通过不涉及肾上腺素受体的机制增强胆碱能神经传递。后者通过不涉及毒蕈碱受体的机制来激发ASM，并且利用细胞内Ca 2+（而不是细胞外Ca 2+）。兴奋-收缩偶联被认为是药物力学性质（而不是机电）。
Thromboxane A2 is believed to participate in causation of hyperreactivity of airway smooth muscle (ASM). We therefore investigated the effects of a thromboxane mimetic (U-46619) on isolated ring segments of canine bronchial ASM (3rd to 5th order). U-46619 (10(-9)-10(-5) M) was found to elicit tonic contraction, membrane depolarization, and oscillations in membrane potential. These effects were sensitive to blockade of thromboxane receptors (using 10(-8) M L 670, 596); the mechanical response was insensitive to 3 x 10(-8) M atropine, 10(-7) M nitrendipine, or exposure to Ca(2+)-free media [(containing 0.5 mM ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA)]. U-46619 also potentiated electrical field stimulation-elicited contractions and excitatory junction potentials without altering the sensitivity to carbachol. This potentiation was also sensitive to L 670,596 but not to blockade of adrenoceptors (using phentolamine plus propranolol). We conclude that canine bronchial ASM possesses both prejunctional and postjunctional thromboxane receptors. The former potentiate cholinergic neurotransmission through a mechanism not involving adrenoceptors. The latter excite the ASM through a mechanism not involving muscarinic receptors and that utilizes intracellular Ca2+ (rather than extracellular Ca2+). Excitation-contraction coupling was found to be pharmacomechanical in nature (rather than electromechanical).