Effects of sodium nitroprusside in the rat cortical collecting duct are independent of the NO pathway.
Effects of sodium nitroprusside in the rat cortical collecting duct are independent of the NO pathway.
复制标题
硝普钠对大鼠皮质集合管的作用与 NO 途径无关。
DOI：
10.1038/ki.1997.64
复制
发表时间：
1997
影响因子：
19.6
通讯作者：
Schlatter,E
中科院分区：
文献类型：
--
作者：
Hirsch,JR;Cermak,R;Forssmann,WG;Kleta,R;Kruhøffer,M;Kuhn,M;Schafer,JA;Sun,D;Schlatter,E
硝普钠在大鼠皮质集合管中的作用不依赖于NO通路，最近我们描述了大鼠皮质集合管（CCD）主细胞基底外侧膜中的K+通道，其由cGMP依赖性蛋白激酶调节（Pflügers Arch 429：338-344，1995）。我们研究了NO释放剂硝普钠（SNP）对大鼠CCD主细胞单通道活性和膜电压（Vm）的影响，以及对离体灌流大鼠CCD小管的跨膜电压、腔-浴Na+通量和渗透水通透性的影响。而在膜片钳实验中，SNP（10μM）使主细胞从-54 ± 10 mV超极化至-71 ± 5 mV（N= 5），并使所述K+通道活性从0.05 ± 0.03增加至0.45 ± 0.14（N= 5），从0.04 ± 0.02增加至0.25 ± 0.05（N- 4）。在离体膜片钳实验中，它对基础或AVP依赖性跨膜电压、Na+通量或渗透水通透性没有影响。此外，50µM SIN-1（另一种NO释放剂）和1 mM L-NAME（一种NO合酶抑制剂）均未显著改变Vm。此外，在cGMP测定中，SNP未能增加CCD片段中的细胞内cGMP。因此，我们的结论是，在大鼠CCD运输不通过NO-途径调节和SNP作为一个cGMP的非依赖性激活剂的K+通道在这些细胞的基底外侧膜。
Effects of sodium nitroprusside in the rat cortical collecting duct are independent of the NO pathway.Recently we described K+channels in the basolateral membrane of principal cells of rat cortical collecting duct (CCD) which are regulated by a cGMP-dependent protein kinase (Pflügers Arch429:338–344, 1995). We examined the effects of the NO-liberator sodium nitroprusside (SNP) on single channel activity and membrane voltage (Vm) in principal cells of rat CCD, and on transepithehal voltage, lumen-to-bath Na+fluxes, and osmotic water permeability in isolated perfused rat CCD tubules. While in patch clamp experiments SNP (10µM) hyperpolarized principal cells from -54 ± 10 mV to -71 ± 5 mV (N= 5) and increased the activity of the described K+channels from 0.05 ± 0.03 to 0.45 ± 0.14 (N= 5) in cell-attached and from 0.04 ± 0.02 to 0.25 ± 0.05 (N- 4) in excised patch clamp experiments, it had no effect on basal or AVP-dependent transepithehal voltage, Na+fluxes, or the osmotic water permeability. In addition, neither 50µM SIN-1, another liberator of NO, nor 1 mM L-NAME, an inhibitor of the NO-synthase, changedVmsignificantly. Furthermore, in cGMP-assays SNP failed to increase intracellular cGMP in CCD segments. Thus, we conclude that in the rat CCD transport is not regulated via the NO-pathway and that SNP acts as an cGMP independent activator of K+channels in the basolateral membrane of these cells.