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雪貂气管腺35SO4-大分子分泌的神经调节。

Neural regulation of 35SO4-macromolecule secretion from tracheal glands of ferrets.

作者信息

Borson D B, Charlin M, Gold B D, Nadel J A

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1984 Aug;57(2):457-66. doi: 10.1152/jappl.1984.57.2.457.

Abstract

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.

摘要

我们的目标是确定哪些神经机制介导雪貂气管黏膜下腺大分子的分泌。为此,我们在有无特定神经阻滞剂和自主神经拮抗剂的情况下,研究了体外35SO4标记的大分子在电刺激或药物刺激下的分泌情况。我们发现,电场刺激以及激动剂乙酰胆碱、去氧肾上腺素、特布他林和去甲肾上腺素均可引起放射性标记物质的分泌。基线期和电刺激后释放的标记物质的分子量大于1000000。单独使用拮抗剂阿托品、酚妥拉明和普萘洛尔分别可阻断对乙酰胆碱、去氧肾上腺素和特布他林的反应,但不影响对其他激动剂的反应,也不改变基线分泌。只有酚妥拉明和普萘洛尔共同作用可阻断对去甲肾上腺素的反应。河豚毒素可阻断对电刺激的反应,但不影响对激动剂的反应。每种拮抗剂均可抑制电刺激反应的很大一部分,但三种拮抗剂联合使用并不能完全阻止分泌。我们得出结论,胆碱能神经通过毒蕈碱机制介导分泌,肾上腺素能神经通过α和β肾上腺素能机制介导分泌,非肾上腺素能-非胆碱能神经通过未知机制介导分泌。

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