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一氧化氮在猫下颌下腺蛋白质分泌调控中的作用。

The role of nitric oxide in the control of protein secretion in the submandibular gland of the cat.

作者信息

Buckle A D, Parker S J, Bloom S R, Edwards A V

机构信息

Physiological Laboratory, University of Cambridge, UK.

出版信息

Exp Physiol. 1995 Nov;80(6):1019-30. doi: 10.1113/expphysiol.1995.sp003899.

DOI:10.1113/expphysiol.1995.sp003899
PMID:8962702
Abstract

Submandibular salivary responses to stimulation of the parasympathetic chorda lingual innervation have been investigated in anaesthetized cats in the presence and absence of N omega-arginine-L-methyl ester (L-NAME) to block the synthesis of nitric oxide. Stimulation either at 2 Hz continuously or at 20 Hz for 1 s at 10 s intervals produced an abrupt fall in submandibular vascular resistance and initiated a flow of submandibular saliva. Neither of these responses differed significantly from the other but the output of protein was significantly potentiated (P < 0.05) when the high-frequency intermittent pattern of stimulation was employed. This potentiation of protein output was abolished in the presence of L-NAME, when the output of protein from the gland was closely similar, whichever pattern of stimulation was employed. Additional administration of atropine completely blocked all submandibular responses to parasympathetic stimulation showing that, in the presence of L-NAME, each response was due to release of acetylcholine acting on muscarinic receptors. The intermittent pattern of chorda lingual nerve stimulation produced a significant rise in the output of vasoactive intestinal peptide (VIP) from the gland (P < 0.01) and this response was significantly reduced following administration of L-NAME (P < 0.05). The results are consistent with the contention that stimulation of the parasympathetic innervation in bursts, which increases the amount of VIP released from the postganglionic nerve terminals, enhances the output of protein in submandibular saliva in the cat. The mechanism involves nitric oxide (NO), which may act, at least in part, presynaptically by modulating VIP release.

摘要

在麻醉猫身上,研究了在存在和不存在Nω-精氨酸-L-甲酯(L-NAME)以阻断一氧化氮合成的情况下,下颌下唾液对副交感舌神经支配刺激的反应。以2Hz连续刺激或以20Hz每秒刺激1次、间隔10秒的方式进行刺激,均会导致下颌下血管阻力突然下降,并引发下颌下唾液分泌。这两种反应之间没有显著差异,但采用高频间歇刺激模式时,蛋白质分泌显著增强(P<0.05)。当使用L-NAME时,蛋白质分泌的这种增强被消除,无论采用何种刺激模式,腺体的蛋白质分泌都非常相似。额外给予阿托品完全阻断了下颌下对副交感神经刺激的所有反应,表明在存在L-NAME的情况下,每种反应都是由于乙酰胆碱作用于毒蕈碱受体而释放所致。舌神经刺激的间歇模式使腺体中血管活性肠肽(VIP)的分泌显著增加(P<0.01),给予L-NAME后,这种反应显著降低(P<0.05)。结果与以下观点一致:阵发性刺激副交感神经支配会增加节后神经末梢释放的VIP量,从而增强猫下颌下唾液中蛋白质的分泌。其机制涉及一氧化氮(NO),它可能至少部分地通过调节VIP释放而在突触前起作用。

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