Grotmol T, Buanes T, Veel T, Roeder M
Institute for Experimental Medical Research, University of Oslo, Norway.
J Intern Med Suppl. 1990;732:47-51.
Ultrastructural studies performed on pigs revealed that numerous cytoplasmic tubulovesicles were present in resting pancreatic duct cells. Elevation of systemic arterial PCO2 from 5.5 to 11 kPa increased the number of vesicles more than twofold. Following secretin administration, concurrent with the onset of HCO3- secretion (JHCO3), the cytoplasm became devoid of vesicles, and the basolateral plasma membrane surface area more than doubled. Similar phenomena were observed in bile duct cells. After pretreatment with the microtubules-inhibiting drug colchicine, secretin failed to reduce duct cell vesicle density, and JHCO3 was reduced by c. 50% compared to the control. These ultrastructural changes resemble those described in other H+/HCO3(-)-transporting organs such as the distal nephron and the urinary bladder. Our findings are compatible with the notion that cytoplasmic vesicles containing H(+)-ATPases are incorporated into the basolateral plasma membrane of secretory cells during secretin stimulation. Active transport of H+ into interstitial fluid might therefore be the driving force underlying JHCO3.
对猪进行的超微结构研究显示，静息状态的胰腺导管细胞中存在大量细胞质微管泡。全身动脉血二氧化碳分压从5.5千帕升高至11千帕，使微管泡数量增加了两倍多。给予促胰液素后，随着碳酸氢根分泌（JHCO3）开始，细胞质中的微管泡消失，基底外侧质膜表面积增加了一倍多。在胆管细胞中也观察到类似现象。用微管抑制药物秋水仙碱预处理后，促胰液素未能降低导管细胞微管泡密度，且JHCO3比对照组降低了约50%。这些超微结构变化类似于在其他氢离子/碳酸氢根转运器官（如远端肾单位和膀胱）中所描述的变化。我们的研究结果与以下观点相符：在促胰液素刺激期间，含有氢离子-ATP酶的细胞质微管泡并入分泌细胞的基底外侧质膜。因此，氢离子向间质液的主动转运可能是JHCO3的潜在驱动力。
