• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Effects on kidney filtration rate by agmatine requires activation of ryanodine channels for nitric oxide generation
【24h】

Effects on kidney filtration rate by agmatine requires activation of ryanodine channels for nitric oxide generation

机译：胍丁胺对肾脏滤过率的影响要求激活用于生成一氧化氮的ryanodine通道

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Agmatine, decarboxylated arginine, is produced in the kidney and can increase nephron and kidney filtration rate via renal vasodilatation and increases in plasma flow. This increase in filtration rate after agmatine is prevented by administration of nitric oxide synthase (NOS) inhibitors. In endothelialcells, agmatine-stimulated nitrite production is accompanied by induction of cytosolic calcium. NOS activity requires calcium for activation; however, the source of this calcium remains unknown. Ryanodine receptor (RyR) calcium-activated calcium release channels are present in the kidney cortex, and we evaluated if RyR contributes to the agmatine response. Agmatine microperfused into Bowman's space reversibly increases nephron filtration rate (SNGFR) by approx 30%. cADP-ribose (cADPR) regulates RyR channel activity. Concurrent infusion of agmatine with the cADPR blocker 8-bromo-cADPR (2 muM) prevents the increase in filtration rate. Furthermore, direct activation of the RyR channel with ryanodine at agonist concentrations (5 muM) increases SNGFR, and, like agmatine, this increase is prevented by administration of N~G-monomethyl-L-arginine, a nonse-lective NOS blocker. We demonstrate that agmatine does not elicit ADPR cyclase activity in vascular smooth muscle membranes and does not directly affect RyR calcium channel responses using sea urchin egg homogenates. These results imply interplay between endothelial cell cADPR/RyR/Ca~(2+)/NO and the cADPR/RyR/Ca~(2+) pathways in vascular smooth muscle cells in arterioles in the regulation of kidney filtration rate. In conclusion, we show that agmatine-induced effects require activation of cADPR and RyR calcium release channels for NO generation, vasodilation, and increased filtration rate.
机译：胍丁胺是一种脱羧精氨酸，在肾脏中产生，可通过肾血管舒张增加肾单位和肾脏滤过率，并增加血浆流量。施用一氧化氮合酶（NOS）抑制剂可防止胍丁胺后过滤速度的增加。在内皮细胞中，胍丁胺刺激的亚硝酸盐产生伴随着胞质钙的诱导。 NOS活性需要钙来激活;但是，这种钙的来源仍然未知。肾皮质中存在Ryanodine受体（RyR）钙激活的钙释放通道，我们评估了RyR是否有助于胍丁胺反应。向鲍曼氏空间微灌注的胍丁胺可逆地将肾单位滤过率（SNGFR）提高约30％。 cADP-核糖（cADPR）调节RyR通道活性。将胍丁胺与cADPR阻滞剂8-溴-cADPR（2μM）同时输注可防止过滤速率的增加。此外，在激动剂浓度（5μM）下用ryanodine直接激活RyR通道可增加SNGFR，并且与胍丁胺一样，可通过使用非选择性NOS阻断剂N〜G-单甲基-L-精氨酸来阻止这种增加。我们证明，胍丁胺不会在血管平滑肌膜中引起ADPR环化酶活性，并且不会直接影响使用海胆卵匀浆的RyR钙通道反应。这些结果暗示小动脉的血管平滑肌细胞中的内皮细胞cADPR / RyR / Ca〜（2 +）/ NO与cADPR / RyR / Ca〜（2+）通路之间的相互作用对肾脏滤过率的调节。总之，我们表明，胍丁胺诱导的效应需要激活cADPR和RyR钙释放通道才能产生NO，扩张血管和增加滤过率。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号