Depletion of secretory granules from the feline parotid gland: action of NANC transmitters per se.
Depletion of secretory granules from the feline parotid gland: action of NANC transmitters per se.
复制标题
猫腮腺分泌颗粒的消耗：NANC 发射器本身的作用。
DOI：
10.1111/j.1748-1716.1994.tb09662.x
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
G. Tobin
中科院分区：
文献类型：
--
作者：
J. Ekström;A. Asztély;H. Helander;G. Tobin
在不存在和存在阿托品的情况下，分别以10 Hz连续刺激副交感耳颞神经90 min后，在戊巴比妥麻醉下的猫中观察到约60%和40%的腮腺腺泡脱粒。阿托品完全消除了腺体对神经刺激的大量液体反应。在非阿托品化猫中，以引起唾液流的剂量率输注至颈动脉中的氨甲酰胆碱与副交感神经刺激相似，导致约25%的腺泡脱粒和腺泡空泡化。血管活性肠肽（VIP; 0.5微克kg-1 min-1也注入颈动脉90 min）引起与拟副交感神经药物相同程度的腺泡脱粒，但该肽未引起任何液体分泌或空泡形成。实验在α-和β-肾上腺素受体阻滞剂存在下进行。因此，在猫的腮腺中，不产生明显的液体分泌，非肾上腺素能、非胆碱能（NANC）机制可能在起作用，引起腺泡颗粒的胞吐作用。这些机制也可能有助于在不阻断经典自主神经受体的情况下响应于副交感神经活动而分泌颗粒。
A parotid acinar degranulation of approximately 60 and 40% was observed in cats under pentobarbitone anaesthesia after a 90-min period of continuous stimulation of the parasympathetic auriculo-temporal nerve at 10 Hz in the absence and presence of atropine, respectively. Atropine completely abolished the large fluid response of the gland to the nerve stimulation. In the non-atropinized cats, bethanechol, infused into the carotid artery at a dose rate evoking a salivary flow similar to that in response to parasympathetic nerve stimulation, caused an acinar degranulation of approximately 25% and acinar vacuolation. Vasoactive intestinal peptide (VIP; 0.5 microgram kg-1 min-1 also infused into the carotid artery for 90 min) caused an acinar degranulation of the same magnitude as the parasympathomimetic drug but the peptide did not give rise to any fluid secretion or vacuole formation. The experiments were performed in the presence of alpha- and beta-adrenoceptor blockers. Thus, in parotid glands of the cat, producing no overt secretion of fluid, non-adrenergic, non-cholinergic (NANC) mechanisms may be at work causing exocytosis of the acinar granules. These mechanisms are also likely to contribute to the secretion of granules in response to parasympathetic nerve activity in the absence of blockade of the classical autonomic receptors.