• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Evidence for a Na+-Ca2+ exchanger in rat pancreatic ducts.

作者信息

Hug M, Pahl C, Novak I

机构信息

Physiologisches Institut, Albert-Ludwigs-Universität, Freiburg, Germany.

出版信息

FEBS Lett. 1996 Nov 18;397(2-3):298-302. doi: 10.1016/s0014-5793(96)01185-4.

DOI:10.1016/s0014-5793(96)01185-4
PMID:8955367
Abstract

Only recently has it been recognized that intracellular Ca2+ is an important cellular mediator in pancreatic ducts. The aim of the present study was to characterize the Ca2+ efflux pathway in ducts freshly prepared from rat pancreas. Lowering of extracellular Na+ concentration resulted in a significant increase in intracellular Ca2+. This effect was fast, reversible, dependent on the extracellular Na+ concentration and did not correlate with intracellular pH changes. It was abolished in Ca2+-free solutions, indicating that the outwardly directed Na+ gradient was directly coupled to a flufenamate insensitive Ca2+ influx. Removal and reintroduction of extracellular Na+ induced transient hyperpolarization and depolarization of Vm, respectively. Taken together, our data indicate that pancreatic ducts possess an electrogenic Na+-Ca2+ exchanger, which under control conditions is responsible for transporting Ca2+ out of resting duct cells.

摘要

相似文献

1
Evidence for a Na+-Ca2+ exchanger in rat pancreatic ducts.
FEBS Lett. 1996 Nov 18;397(2-3):298-302. doi: 10.1016/s0014-5793(96)01185-4.
2
Calcium influx pathways in rat pancreatic ducts.
Pflugers Arch. 1996 Jun;432(2):278-85. doi: 10.1007/s004240050134.
3
Regulation of the Na+/Ca2+ exchanger in rat pancreatic ducts.
J Membr Biol. 2002 Mar 1;186(1):43-53. doi: 10.1007/s00232-001-0134-x.
4
Kinetic properties of the sodium-calcium exchanger in rat brain synaptosomes.大鼠脑突触体中钠钙交换体的动力学特性
J Physiol. 1995 Jun 1;485 ( Pt 2)(Pt 2):349-64. doi: 10.1113/jphysiol.1995.sp020734.
5
Involvement of the glutamate transporter and the sodium-calcium exchanger in the hypoxia-induced increase in intracellular Ca2+ in rat hippocampal slices.谷氨酸转运体和钠钙交换体在大鼠海马切片缺氧诱导的细胞内钙离子增加中的作用。
Brain Res. 1998 Dec 7;813(2):351-8. doi: 10.1016/s0006-8993(98)01037-3.
6
Contribution of Na+/Ca2+ exchanger in maintaining [Ca2+]c at a stable state in rat pancreatic islets.钠/钙交换体在维持大鼠胰岛细胞质钙离子浓度处于稳定状态中的作用。
Jpn J Physiol. 1996 Dec;46(6):473-80. doi: 10.2170/jjphysiol.46.473.
7
Bepridil exacerbates glutamate-induced deterioration of calcium homeostasis and cultured nerve cell injury.
Int J Neurosci. 1996 Dec;88(3-4):199-214. doi: 10.3109/00207459609000615.
8
Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger.哺乳动物中枢神经系统白质缺氧损伤的离子机制:钠离子通道和钠钙交换体的作用
J Neurosci. 1992 Feb;12(2):430-9. doi: 10.1523/JNEUROSCI.12-02-00430.1992.
9
Mechanisms of injury-induced calcium entry into peripheral nerve myelinated axons: role of reverse sodium-calcium exchange.损伤诱导钙进入周围神经有髓轴突的机制:反向钠钙交换的作用
J Neurochem. 1996 Feb;66(2):493-500. doi: 10.1046/j.1471-4159.1996.66020493.x.
10
The origin of increased cytoplasmic calcium upon reversal of the Na+/Ca(2+)-exchanger in isolated rat ventricular myocytes.离体大鼠心室肌细胞中钠/钙交换体反转时细胞质钙增加的起源。
J Mol Cell Cardiol. 1996 Sep;28(9):1963-73. doi: 10.1006/jmcc.1996.0189.

引用本文的文献

1
Glycolytic ATP fuels the plasma membrane calcium pump critical for pancreatic cancer cell survival.糖酵解产生的 ATP 为质膜钙泵供能,这对胰腺癌细胞的存活至关重要。
J Biol Chem. 2013 Dec 13;288(50):36007-19. doi: 10.1074/jbc.M113.502948. Epub 2013 Oct 24.
2
Sequence motifs in adenoviral DNA block immune activation by stimulatory CpG motifs.腺病毒DNA中的序列基序可阻断刺激性CpG基序引发的免疫激活。
Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12631-6. doi: 10.1073/pnas.95.21.12631.