AQP and the control of fluid transport in a salivary gland
AQP and the control of fluid transport in a salivary gland
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DOI：
10.1007/s00232-005-0848-2
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发表时间：
2006-03-01
影响因子：
2.4
通讯作者：
Hill, A. E.
中科院分区：
文献类型：
--
作者：
Murakami, M.;Murdiastuti, K.;Hill, A. E.
用大鼠颌下腺体外灌流实验，通过改变源浴的渗透压和观察分泌体积流量的变化来探讨盐水耦合的性质。通过将生理盐水灌流液改变为含有不同水平蔗糖的灌流液，腺体经历了高渗阶梯变化。流速下降到一个较低的值，建立了一个新的稳态流动。这一速率变化与液体产生是由于简单的渗透平衡而产生的系统的预期不一致，但要大得多。这些变化符合一个模型，在该模型中，液体产生在很大程度上是旁细胞的，其速度由基底膜中的渗透传感器系统控制。同样的实验也是用来自大鼠的腺体进行的，这些大鼠的腺体中AQP5(唾液腺泡细胞的主要水通道蛋白)水平非常低，其中AQP5在基底膜上几乎没有表达。在这些大鼠中，高渗刺激后的唾液分泌速率很小，最好的模型是简单的渗透平衡。在AQP5水平中等的大鼠，虽然AQP5水平降低，但其流率变化与正常大鼠相似。最后，灌流的正常腺体在根尖腺泡膜逆行注射含有不同水平Hg2+离子(0、10和100微米)的生理盐水，这些生理盐水将作为AQP5的抑制剂。随着Hg2+浓度的升高，总流率逐渐减小，但在高渗刺激后，流率的变化不变，与正常大鼠相似。所有这些结果都很难用细胞渗透模型解释，但可以用基底膜上存在的渗透传感器(可能是AQP5)控制细胞旁流的模型来解释。
Experiments were performed with the perfused rat submandibular gland in vitro to investigate the nature of the coupling between transported salt and water by varying the osmolarity of the source bath and observing the changes in secretory volume flow. Glands were submitted to hypertonic step changes by changing the saline perfusate to one containing different levels of sucrose. The flow rate responded by falling to a lower value, establishing a new steady-state flow. The rate changes did not correspond to those expected from a system in which fluid production is due to simple osmotic equilibration, but were much larger. The changes were fitted to a model in which fluid production is largely paracellular, the rate of which is controlled by an osmosensor system in the basal membrane. The same experiments were done with glands from rats that had been bred to have very low levels of AQP5 (the principal aquaporin of the salivary acinar cell) in which little AQP5 is expressed at the basal membrane. In these rats, salivary secretion rates after hypertonic challenges were small and best modelled by simple osmotic equilibration. In rats which had intermediate AQP5 levels the changes in flow rate were similar to those of normal rats although their AQP5 levels were reduced.Finally, perfused normal glands were subject to retrograde ductal injection of salines containing different levels of Hg2+ ions (0, 10 and 100 mu m) which would act as inhibitors of AQP5 at the apical acinar membrane. The overall flow rates were progressively diminished with rising Hg2+ concentration, but after hypertonic challenge the changes in flow rates were unchanged and similar to those of normal rats.All these results are difficult to explain by a cellular osmotic model but can be explained by a model in which paracellular flow is controlled by an osmosensor (presumably AQP5) present on the basal membrane.