Regulation of Na-transporters by steroid hormones : genomic and non-genomic actions

我们使用的皮质收集管（CCD）从兔肾脏和培养的血管平滑肌细胞（VSMC），以确定钠转运（钠泵，钠/氢交换器，和上皮钠通道）的类固醇激素的影响，其基因组和非基因组行动。结果表明：（1）在CCD中，基底外侧钾浓度从2.5 ~ 8.5mM急剧升高激活了基底外侧钠泵，从而使顶端Na和K电导升高。DOCA预处理增加了基底外侧钾电导，并增强了基底外侧钠泵活性和顶端阳离子电导对钾升高的反应。腔钠浓度的变化，细胞钠浓度，调制之间的紧密耦合的基底外侧钠泵和顶端阳离子电导; 2）在CCD从对照兔，提高腔钠浓度从14至147 mM激活基底外侧钠泵和顶端Na和K电导通过增加细胞Na浓度。在DOCA处理的兔CCD中，基底外侧泵和顶端阳离子电导的腔Na依赖性激活急剧增强。慢性DOCA预处理也增加了基底外侧K电导后，管腔Na浓度升高; 3）在VSMC中，醛固酮激活Na/H交换（NHE）的非基因组和基因组机制; 4）在VSMC中，皮质酮激活NHE的非基因组机制，但抑制它，基因组机制。

We used the cortical collecting duct (CCD) from rabbit kidneys and cultured vascular smooth muscle cells (VSMC) to determine the effects of steroid hormones on Na-transporters (Na pump, Na/H exchanger, and epithelial Na channel) in terms of their genomic and non-genomic actions. The results were in the following :1) In the CCD, acute elevation of basolateral K concentrations from 2.5 to 8.5 mM activated the basolateral Na pump, which secondarily elevates the apical Na and K conductances. DOCA pretreatment increased the basolateral K conductances and augmented the response to the rise of K of both the basolateral Na pump activity and the apical cation conductances. Luminal Na concentration, by changes in cell Na concentrations, modulated the tight coupling between the basolateral Na pump and apical cation conductances; 2) In the CCD from control rabbits, raising luminal Na concentrations from 14 to 147 mM activated basolateral Na pump and apical Na and K conductances via increased cell Na concentrations. The luminal Na-dependent activation of the basolateral pump and the apical cation conductances was sharply enhanced in the CCD from DOCA-treated rabbits. Chronic DOCA pretreatment also increased basolateral K conductance upon raising luminal Na concentration; 3) In VSMC, aldosterone activated Na/H exchange (NHE) by nongenomic and genomic mechanisms; 4) In VSMC, corticosterone activated NHE by nongenomic mechanisms, but inhibited it, by genomic mechanisms.