Romell B, Girma K, Seensalu R, Nilsson G
Dept. of Physiology, Swedish University of Agricultural Sciences, College of Veterinary Medicine, Uppsala.
Scand J Gastroenterol. 1993 Jun;28(6):545-50. doi: 10.3109/00365529309098264.
The present study examines the possible existence of a mechanism regulating emptying of the secretory canaliculi content of the parietal cell and the possible effects of carbachol and gastrin on such a mechanism. In rabbit gastric glands stimulated with carbachol, 14C-aminopyrine accumulation reached a maximum after 15 min and then started to decrease. This decrease was not accompanied by a decrease in oxygen consumption, nor was any decrease of accumulated 14C-aminopyrine seen in dispersed gastric cells. In glands but not in cells stimulated with histamine together with 3-isobutyl-1-methylxanthine (IMX), carbachol induced a reduction in the accumulated 14C-aminopyrine content, whereas the effect of gastrin was less pronounced. The carbachol-induced reduction was counteracted by atropine but was not accompanied by a decrease in oxygen consumption. It is suggested that there exists a mechanism that controls the emptying of the secretory canaliculi content of the parietal cell, and that carbachol, in addition to stimulating acid production, also contributes to this emptying. Paracrine factors may be involved in this latter mechanism.
本研究探讨了壁细胞分泌小管内容物排空调节机制的可能存在,以及卡巴胆碱和胃泌素对该机制的可能影响。在用卡巴胆碱刺激的兔胃腺中,14C-氨基比林的积累在15分钟后达到最大值,然后开始下降。这种下降并未伴随氧消耗的减少,在分散的胃细胞中也未观察到积累的14C-氨基比林有任何减少。在用组胺和3-异丁基-1-甲基黄嘌呤(IMX)刺激的腺体而非细胞中,卡巴胆碱导致积累的14C-氨基比林含量降低,而胃泌素的作用则不太明显。卡巴胆碱诱导的降低被阿托品抵消,但并未伴随氧消耗的减少。提示存在一种控制壁细胞分泌小管内容物排空的机制,并且卡巴胆碱除了刺激酸分泌外,还促进这种排空。旁分泌因子可能参与了后一种机制。