• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Activation of particulate guanylyl cyclase by endothelins in cultured SV-40 transformed cat iris sphincter smooth muscle cells.
【24h】

Activation of particulate guanylyl cyclase by endothelins in cultured SV-40 transformed cat iris sphincter smooth muscle cells.

机译：在培养的SV-40转化的猫虹膜括约肌平滑肌细胞中，内皮素激活了鸟嘌呤环化酶颗粒。

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

We investigated the effects of endothelins (ETs) on cGMP production in cultured SV-40 transformed cat iris sphincter smooth muscle (SV-CISM-2) cells. ET-3 increased cGMP formation in a concentration-dependent manner (EC50 = 98nM), which was 2.5 times higher than that of ET-1. The ET(B)receptor agonists sarafotoxin-S6c and IRL 1620 also increased cGMP production, mimicking the effects of the ETs. The ET(B) receptor antagonist BQ 788, but not the ET(A) receptor antagonist BQ610, dose-dependently blocked ET-3-stimulated cGMP formation (IC50=10nM). The phorbol ester, Phorbol 12, 13-dibutyrate (PDBu), which inhibits particulate guanylyl cyclase in smooth muscle, dose-dependently inhibited ET-3-stimulated cGMP accumulation (IC50=66nM). LY83583 and ODQ, inhibitors of soluble guanylyl cyclases, as well as inhibitors of the nitric oxide cascade and of intracellular Ca2+ elevation had no appreciable effect on ET-3-induced cGMP production. ET-3 markedly inhibited carbachol-induced intracellular Ca2+ mobilization. We conclude that ET-3 increases intracellular cGMP levels in SV-CISM-2 cells through activation of the ET(B) receptor subtype and subsequent stimulation of the membrane-bound guanylyl cyclase. Elevation of cGMP by ET and the subsequent inhibition of muscarinic stimulation of intracellular Ca2+ mobilization by the cyclic nucleotide could serve to modulate the contractile effects of Ca2+-mobilizing agonists in the iris sphincter smooth muscle.
机译：我们调查了内皮素（ETs）对培养的SV-40转化猫虹膜括约肌平滑肌（SV-CISM-2）细胞中cGMP产生的影响。 ET-3以浓度依赖性方式增加cGMP的形成（EC50 = 98nM），是ET-1的2.5倍。 ET（B）受体激动剂sarafotoxin-S6c和IRL 1620也增加了cGMP的产生，模仿了ET的作用。 ET（B）受体拮抗剂BQ 788，而不是ET（A）受体拮抗剂BQ610，剂量依赖性地阻断了ET-3刺激的cGMP的形成（IC50 = 10nM）。佛波酯，Phorbol 12，13-dibutyrate（PDBu），抑制平滑肌中的鸟嘌呤环化酶颗粒，剂量依赖性地抑制了ET-3刺激的cGMP积累（IC50 = 66nM）。 LY83583和ODQ，可溶性鸟苷酰环化酶的抑制剂，一氧化氮级联和细胞内Ca2 +升高的抑制剂，对ET-3诱导的cGMP产生没有明显影响。 ET-3明显抑制卡巴胆碱诱导的细胞内Ca2 +动员。我们得出的结论是，ET-3通过激活ET（B）受体亚型和随后刺激膜结合鸟苷酸环化酶来增加SV-CISM-2细胞中的细胞内cGMP水平。 ET引起cGMP的升高以及随后环环核苷酸抑制毒蕈碱刺激细胞内Ca2 +动员的作用可以调节Ca2 +动员激动剂在虹膜括约肌平滑肌中的收缩作用。

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