Yamamoto T, Sasaki S, Fushimi K, Ishibashi K, Yaoita E, Kawasaki K, Marumo F, Kihara I
Department of Pathology, Niigata University School of Medicine, Japan.
Am J Physiol. 1995 Jun;268(6 Pt 1):C1546-51. doi: 10.1152/ajpcell.1995.268.6.C1546.
The effect of vasopressin on subcellular localization of AQP-CD and AQP3 water channels was examined in thirsted Brattleboro rats by immunohistochemistry and immunoelectron microscopy. AQP-CD was mainly present in the cytoplasm of the collecting duct cells in association with cytoplasmic vesicles but was sparse in the apical membrane in control vehicle-injected rats. In rats given vasopressin 15 min before death, the number of immunogold particles for AQP-CD in the apical membrane increased significantly (P < 0.002) from 1.8 +/- 0.2 to 10.0 +/- 0.4/microns with a significant decrease (P < 0.05) of cytoplasmic labeling from 32.6 +/- 6.4 to 24.6 +/- 5.6/microns 2, indicating that AQP-CD is the vasopressin-regulated water channel predicted by the "shuttle" hypothesis. In contrast, AQP3 was restricted to the basolateral membrane of the collecting duct cells, and the labeling density of AQP3 was unchanged by vasopressin treatment, indicating that AQP3 is constitutively expressed and may maintain high water permeability of the basolateral membrane.
通过免疫组织化学和免疫电子显微镜检查,研究了加压素对缺水的布拉特洛维大鼠中AQP-CD和AQP3水通道亚细胞定位的影响。在对照的注射溶媒的大鼠中,AQP-CD主要存在于集合管细胞的细胞质中,与细胞质囊泡相关,但在顶端膜中稀少。在死亡前15分钟给予加压素的大鼠中,顶端膜中AQP-CD的免疫金颗粒数量从1.8±0.2显著增加至10.0±0.4/μm(P<0.002),细胞质标记从32.6±6.4显著减少至24.6±5.6/μm²(P<0.05),表明AQP-CD是“穿梭”假说预测的加压素调节的水通道。相反,AQP3局限于集合管细胞的基底外侧膜,加压素处理后AQP3的标记密度未改变,表明AQP3是组成性表达的,可能维持基底外侧膜的高水渗透性。