Neural regulation of 35SO4-macromolecule secretion from tracheal glands of ferrets.
Neural regulation of 35SO4-macromolecule secretion from tracheal glands of ferrets.
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雪貂气管腺35SO4-大分子分泌的神经调节。
DOI：
10.1152/jappl.1984.57.2.457
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Nadel,JA
中科院分区：
文献类型：
--
作者：
Borson,DB;Charlin,M;Gold,BD;Nadel,JA
我们的目标是确定是什么神经机制介导的大分子物质分泌的气管粘膜下腺的雪貂。要做到这一点，我们研究了35 SO 4-标记的大分子在体外的电刺激或药物刺激的情况下，存在和不存在一个特定的神经阻滞剂和自主神经拮抗剂的分泌。我们发现，电场刺激和激动剂乙酰胆碱，phenylethyl，特布他林，和去甲肾上腺素各自引起放射性标记物质的分泌。基线期间和电刺激后释放的标记材料的分子量大于1，000，000。拮抗剂阿托品，酚妥拉明，普萘洛尔单独防止乙酰胆碱，苯肾上腺素，特布他林，分别，而不阻止任何其他这些激动剂的反应或改变基线分泌。只有酚妥拉明和普萘洛尔一起阻止了对去甲肾上腺素的反应。河豚毒素阻止对电刺激的反应，但不阻止对激动剂的反应。每一种拮抗剂都抑制了对电刺激的反应的很大一部分，但所有三种拮抗剂的组合并不能完全阻止分泌。我们的结论是，胆碱能神经介导分泌通过毒蕈碱机制，肾上腺素能神经介导分泌通过α和β-肾上腺素能机制，和非肾上腺素能非胆碱能神经介导分泌通过不明机制。
Our goal was to determine what nervous mechanisms mediate the secretion of macromolecules from tracheal submucosal glands of ferrets. To do this, we studied the secretion of 35SO4-labeled macromolecules in vitro in response to electrical or pharmacological stimulation in the absence and presence of a specific nerve blocker and autonomic antagonists. We found that electrical field stimulation and the agonists acetylcholine, phenylephrine, terbutaline, and norepinephrine each cause secretion of radiolabeled materials. The molecular weights of the labeled materials released during base line and after electrical stimulation were greater than 1,000,000. The antagonists atropine, phentolamine, and propranolol alone prevented the responses to acetylcholine, phenylephrine, and terbutaline, respectively, without preventing responses to any other of these agonists or changing baseline secretion. Only phentolamine and propranolol together prevented the response to norepinephrine. Tetrodotoxin prevented the response to electrical stimulation but not the responses to the agonists. Each of the antagonists inhibited a significant portion of the response to electrical stimulation, but the combination of all three did not completely prevent secretion. We conclude that cholinergic nerves mediate secretion via muscarinic mechanisms, that adrenergic nerves mediate secretion via both alpha- and beta-adrenergic mechanisms, and that nonadrenergic-noncholinergic nerves mediate secretion via unidentified mechanisms.