Suppr超能文献

异喹啉衍生物LOE 908对人内皮细胞中一种钙库操纵的钙离子内流途径的抑制作用。

Inhibition of a store-operated Ca2+ entry pathway in human endothelial cells by the isoquinoline derivative LOE 908.

作者信息

Encabo A, Romanin C, Birke F W, Kukovetz W R, Groschner K

机构信息

Institut für Pharmakologie and Toxikologie, Karl-Franzens-Universităt Graz, Austria.

出版信息

Br J Pharmacol. 1996 Oct;119(4):702-6. doi: 10.1111/j.1476-5381.1996.tb15729.x.

Abstract
  1. The novel cation channel blocker, LOE 908, was tested for its effects on Ca2+ entry and membrane currents activated by depletion of intracellular Ca2+ stores in human endothelial cells. 2. LOE 908 inhibited store-operated Ca2+ entry induced by direct depletion of Ca2+ stores with 100 nM thapsigargin or 100 nM ionomycin with an EC50 of 2 microM and 4 microM, respectively. 3. LOE 908 did not affect thapsigargin- or ionomycin-induced Ca2+ release from intracellular stores up to concentrations of 3 microM. 4. LOE 908 reversibly suppressed thapsigargin- as well as ionomycin-induced whole-cell membrane currents. 5. The LOE 908-sensitive membrane conductance corresponded to a cation permeability of 5.5 and 6.9 fold selectivity for Ca2+ over K+ in the presence of thapsigargin and ionomycin, respectively. 6. Our results suggest that the isoquinoline, LOE 908 is a novel, potent inhibitor of the store-operated (capacitive) Ca2+ entry pathway in endothelial cells.
摘要
  1. 新型阳离子通道阻滞剂LOE 908,被测试其对人内皮细胞中细胞内钙库耗竭所激活的钙内流和膜电流的影响。2. LOE 908抑制由100 nM毒胡萝卜素或100 nM离子霉素直接耗竭钙库所诱导的钙库操纵性钙内流,其半数有效浓度(EC50)分别为2 microM和4 microM。3. 高达3 microM的浓度时,LOE 908不影响毒胡萝卜素或离子霉素诱导的细胞内钙库钙释放。4. LOE 908可逆地抑制毒胡萝卜素以及离子霉素诱导的全细胞膜电流。5. 在存在毒胡萝卜素和离子霉素的情况下,LOE 908敏感的膜电导分别对应于对Ca2+的阳离子通透性,相对于K+对Ca2+的选择性为5.5倍和6.9倍。6. 我们的结果表明,异喹啉类化合物LOE 908是内皮细胞中钙库操纵性(电容性)钙内流途径的一种新型强效抑制剂。

相似文献

引用本文的文献

5
Calcium channels activated by endothelin-1 in human trophoblast.人滋养层细胞中由内皮素-1激活的钙通道。
J Physiol. 2004 Dec 1;561(Pt 2):449-58. doi: 10.1113/jphysiol.2004.073023. Epub 2004 Sep 9.

本文引用的文献

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验