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神经肽Y抑制大鼠尾动脉血管平滑肌细胞中的钙激活钾通道。

Neuropeptide Y inhibits Ca(2+)-activated K+ channels in vascular smooth muscle cells from the rat tail artery.

作者信息

Xiong Z, Cheung D W

机构信息

University of Ottawa Heart Institute, Canada.

出版信息

Pflugers Arch. 1994 Dec;429(2):280-4. doi: 10.1007/BF00374324.

Abstract

The effects of neuropeptide Y (NPY) on the Ca(2+)-activated K+ channel in smooth muscle cells from the rat tail artery were studied by whole-cell and single-channel patch-clamp recording techniques. In the presence of nifedipine (1 microM), whole-cell outward currents through Ca(2+)-activated K+ channels were inhibited by NPY in a dose-dependent manner from 20 to 200 nM. A maximum inhibition to about 48% of the control current could be achieved. Recordings from outside-out patches showed that the open probability of Ca(2+)-activated K+ channels were similarly inhibited by NPY. At 200 nM NPY, the open probability was reduced to about 36% of the control value. NPY did not affect the open times or current amplitude, but increased significantly the short (from 0.49 to 0.58 ms) and long (from 441 to 728 ms) closed times. Inhibition of Ca(2+)-activated K+ channels by NPY may contribute to its excitatory action on vascular smooth muscle cells.

摘要

采用全细胞膜片钳和单通道膜片钳记录技术,研究了神经肽Y(NPY)对大鼠尾动脉平滑肌细胞中钙激活钾通道的影响。在硝苯地平(1微摩尔)存在的情况下,通过钙激活钾通道的全细胞外向电流被NPY以剂量依赖的方式抑制,浓度范围为20至200纳摩尔。最大抑制可达对照电流的约48%。从外侧向外膜片的记录显示,钙激活钾通道的开放概率同样被NPY抑制。在200纳摩尔NPY作用下,开放概率降至对照值的约36%。NPY不影响开放时间或电流幅度,但显著增加了短关闭时间(从0.49毫秒增加到0.58毫秒)和长关闭时间(从441毫秒增加到728毫秒)。NPY对钙激活钾通道的抑制作用可能有助于其对血管平滑肌细胞的兴奋作用。

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