Civan M M, Frazier H S
J Gen Physiol. 1968 May;51(5):589-605. doi: 10.1085/jgp.51.5.589.
Vasopressin increases the net transport of sodium across the isolated urinary bladder of the toad by increasing the mobility of sodium ion within the tissue. This change is reflected in a decreased DC resistance of the bladder; identification of the permeability barrier which is affected localizes the site of action of vasopressin on sodium transport. Cells of the epithelial layer were impaled from the mucosal side with glass micropipettes while current pulses were passed through the bladder. The resulting voltage deflections across the bladder and between the micropipette and mucosal reference solution were proportional to the resistance across the entire bladder and across the mucosal or apical permeability barrier, respectively. The position of the exploring micropipette was not changed and vasopressin was added to the serosal medium. In 10 successful impalements, the apical permeability barrier contributed 54% of the initial total transbladder resistance, but 98% of the total resistance change following vasopressin occurred at this site. This finding provides direct evidence that vasopressin acts to increase ionic mobility selectively across the apical permeability barrier of the transporting cells of the toad bladder.
血管加压素通过增加钠离子在组织内的移动性,提高了蟾蜍离体膀胱对钠的净转运。这种变化反映在膀胱直流电阻降低;确定受影响的渗透屏障可定位血管加压素对钠转运的作用位点。用玻璃微电极从黏膜侧刺入上皮层细胞,同时向膀胱施加电流脉冲。由此产生的横跨膀胱以及微电极与黏膜参比溶液之间的电压偏转分别与整个膀胱以及黏膜或顶端渗透屏障的电阻成正比。探索性微电极的位置不变,将血管加压素添加到浆膜介质中。在10次成功的刺入实验中,顶端渗透屏障占初始总跨膀胱电阻的54%,但血管加压素作用后总电阻变化的98%发生在该部位。这一发现提供了直接证据,表明血管加压素的作用是选择性地增加蟾蜍膀胱转运细胞顶端渗透屏障的离子移动性。