Wright R D, Blair-West J R
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria, Australia.
Exp Physiol. 1990 May;75(3):339-48. doi: 10.1113/expphysiol.1990.sp003408.
The vascularly isolated parotid glands of sheep were submaximally stimulated for 4 min by nerve stimulation, or by infusion of acetylcholine (ACh) or bethanechol directly into the artery supplying the gland. The three modes of stimulation caused almost equal increases in the rate of salivary flow, initial losses of K+ and phosphate from the gland and total glandular deficits of K+ and phosphate. Concurrent arterial infusion of the K+ channel blocker tetraethylammonium (TEA), at 1.5-3.3 mM in blood, almost abolished these responses to bethanechol but did not alter the responses to nerve stimulation or ACh. The responses to bethanechol were restored by increasing the concentration fourfold. Concurrent arterial infusion of 4-aminopyridine (4-AP), at 0.1-2.3 mM in blood, partially inhibited the increase in salivary flow due to bethanechol but not the response to nerve stimulation or ACh. The specificity and competitive nature of the action of TEA and 4-AP on responses to direct muscarinic stimulation by bethanechol are consistent with blockade of K+ channels in secretory end-piece cells. The failure of TEA and 4-AP to inhibit responses to nerve stimulation and ACh may be due to the blocking agents potentiating the release of neurotransmitter ACh. It is also possible that nerve stimulation and ACh may cause the release of a co-transmitter which bethanechol does not.
对绵羊的血管分离腮腺进行亚最大刺激4分钟，刺激方式为神经刺激，或直接向供应腺体的动脉中注入乙酰胆碱（ACh）或氨甲酰甲胆碱。这三种刺激方式导致唾液分泌速率几乎同等增加，腺体中钾离子和磷酸盐的初始流失以及腺体中钾离子和磷酸盐的总缺失。同时在血液中以1.5 - 3.3 mM的浓度动脉注入钾离子通道阻滞剂四乙铵（TEA），几乎消除了对氨甲酰甲胆碱的这些反应，但未改变对神经刺激或ACh的反应。将浓度增加四倍可恢复对氨甲酰甲胆碱的反应。同时在血液中以0.1 - 2.3 mM的浓度动脉注入4 - 氨基吡啶（4 - AP），部分抑制了由氨甲酰甲胆碱引起的唾液分泌增加，但未抑制对神经刺激或ACh的反应。TEA和4 - AP对氨甲酰甲胆碱直接毒蕈碱刺激反应的作用的特异性和竞争性性质与分泌终末细胞中钾离子通道的阻断一致。TEA和4 - AP未能抑制对神经刺激和ACh的反应可能是由于阻断剂增强了神经递质ACh的释放。也有可能神经刺激和ACh可能导致释放一种氨甲酰甲胆碱不会释放的共递质。
