Atrial natriuretic factor and cGMP inhibit amiloride-sensitive Na+ transport in the cultured renal epithelial cell line, LLC-PK1.
Atrial natriuretic factor and cGMP inhibit amiloride-sensitive Na+ transport in the cultured renal epithelial cell line, LLC-PK1.
复制标题
心房钠尿因子和 cGMP 抑制培养的肾上皮细胞系 LLC-PK1 中阿米洛利敏感的 Na 转运。
DOI：
10.1016/s0006-291x(86)80498-3
复制
发表时间：
1986
影响因子：
3.1
通讯作者：
Ausiello,DA
中科院分区：
文献类型：
--
作者：
Cantiello,HF;Ausiello,DA
利用肾细胞培养模型lc - pk1，研究了心房肽肽II和cGMP对上皮细胞Na+转运的直接影响，该模型含有一个对阿米洛利敏感的传导Na+转运途径和一个Na+/H+交换器。将细胞暴露于atriopeptin II（10−7M）中，在加入单层细胞的2分钟内增加了cGMP的产生。Atriopeptin II（10−7M）或外源性8-溴- cgmp（10−3M）通过传导途径最大限度地抑制22na +的摄取，占22na +总摄取的60%。atriopeptin II对这种抑制作用的表观ki值为2 × 10−11M。阿米洛利抑制22na +摄取的程度与阿特里opeptin II相似，两种药物的作用并不是叠加的。相比之下，atriopeptin II和cGMP都没有减弱pH梯度诱导的22na +摄取的增加。因此，atriopeptin II可能通过刺激cGMP直接抑制Na+在肾上皮细胞中的转运。
The renal cell culture model, LLC-PK1, which contains an amiloride-sensitive conductive Na+transport pathway and a Na+/H+exchanger, was utilized to examine the direct effects of atriopeptin II and cGMP on Na+transport in epithelial cells. Exposure of cells to atriopeptin II (10−7M) increased cGMP production within 2 min of addition to cells in monolayer. Atriopeptin II (10−7M) or exogenous 8-bromo-cGMP (10−3M) maximally inhibited the uptake of22Na+through the conductive pathway which accounted for up to 60% of total22Na+uptake. The apparent Kifor this inhibition by atriopeptin II was 2 × 10−11M. Amiloride inhibited22Na+uptake to a similar extent as atriopeptin II, and the effects of the presence of both agents was not additive. In contrast, neither atriopeptin II nor cGMP blunted the increment in22Na+uptake induced by a pH gradient. Thus atriopeptin II can directly inhibit Na+transport in renal epithelial cells, probably through its stimulation of cGMP.