Fox J E, Daniel E E, Jury J, Track N S, Chiu S
Can J Physiol Pharmacol. 1982 Jul;60(7):893-901. doi: 10.1139/y82-126.
We used acute anesthetized dogs to investigate the role of cholinergic receptors in the relationship between antral immunoreactive (I) gastrin release and antral motility. Electrical stimulation of extrinsic nerves via the cervical vagus or the nerve of Latarjet appeared to increase I gastrin release and antral motility by separate pathways as blockade of muscarinic receptors, i.e., atropinization inhibited motility but did not alter I gastrin release. On the other hand, blockade of nicotinic receptors by hexamethonium treatment obliterated I gastrin release induced by stimulation of the extrinsic nerves but only reduced motility. Field stimulation of intrinsic nerves via serosal electrodes also increased both I gastrin release and local motility. Since hexamethonium treatment only slightly reduced both I gastrin release and motility and atropinization eliminated both during field stimulation, the presence of a muscarinic receptor in the final pathway for each is proposed. Atropine eliminated carbachol-induced I gastrin release and motility increases, even in the presence of nerve blockade by tetrodotoxin. This suggests that this muscarinic receptor is on the smooth muscle cell itself and possibly on the gastrin cell. However a proposed role of the somatostatin cell in controlling gastrin release is also consistent with these data. Thus, both an intrinsic cholinergic and a separate extrinsic noncholinergic pathway are involved in antral release of I gastrin but initiation of motility appears to involve a final common pathway terminating in a muscarinic receptor on the smooth muscle cell.
我们使用急性麻醉的犬来研究胆碱能受体在胃窦免疫反应性（I）胃泌素释放与胃窦运动之间关系中的作用。通过颈迷走神经或拉塔热神经对内脏神经进行电刺激，似乎通过不同途径增加了I胃泌素释放和胃窦运动，因为毒蕈碱受体的阻断，即阿托品化抑制了运动，但并未改变I胃泌素释放。另一方面，六甲铵处理阻断烟碱受体消除了由内脏神经刺激诱导的I胃泌素释放，但仅降低了运动。通过浆膜电极对内在神经进行场刺激也增加了I胃泌素释放和局部运动。由于六甲铵处理仅轻微降低了I胃泌素释放和运动，而阿托品化在进行场刺激时消除了两者，因此推测在各自的最终途径中存在毒蕈碱受体。即使在存在河豚毒素引起的神经阻滞的情况下，阿托品也消除了卡巴胆碱诱导的I胃泌素释放和运动增加。这表明该毒蕈碱受体存在于平滑肌细胞本身，也可能存在于胃泌素细胞上。然而，生长抑素细胞在控制胃泌素释放中所起的作用也与这些数据一致。因此，内在胆碱能途径和独立的外在非胆碱能途径均参与了胃窦I胃泌素的释放，但运动的启动似乎涉及一个最终共同途径，该途径终止于平滑肌细胞上的毒蕈碱受体。
