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高细胞外钾离子浓度对新鲜分离的兔尿道Cajal间质细胞中自发钙波的影响。

The effect of high [K(+)]o on spontaneous Ca(2+) waves in freshly isolated interstitial cells of Cajal from the rabbit urethra.

作者信息

Drumm Bernard T, Sergeant Gerard P, Hollywood Mark A, Thornbury Keith T, Matsuda Toshio T, Baba Akemichi, Harvey Brian J, McHale Noel G

机构信息

Smooth Muscle Research Centre, Dundalk Institute of Technology, DundalkCo. Louth, Ireland ; Department of Molecular Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin 9, Ireland.

Smooth Muscle Research Centre, Dundalk Institute of Technology, DundalkCo. Louth, Ireland.

出版信息

Physiol Rep. 2014 Jan 21;2(1):e00203. doi: 10.1002/phy2.203. eCollection 2014 Jan 1.

Abstract

Interstitial cells of Cajal (ICC) act as putative pacemaker cells in the rabbit urethra. Pacemaker activity in ICC results from spontaneous global Ca(2+) waves that can be increased in frequency by raising external [K(+)]. The purpose of this study was to elucidate the mechanism of this response. Intracellular [Ca(2+)] was measured in fluo-4-loaded smooth muscle cells (SMCs) and ICC using a Nipkow spinning disk confocal microscope. Increasing [K(+)]o to 60 mmol/L caused an increase in [Ca(2+)]i accompanied by contraction in SMCs. Raising [K(+)]o did not cause contraction in ICC, but the frequency of firing of spontaneous calcium waves increased. Reducing [Ca(2+)]o to 0 mmol/L abolished the response in both cell types. Nifedipine of 1 μmol/L blocked the response of SMC to high [K(+)]o, but did not affect the increase in firing in ICC. This latter effect was blocked by 30 μmol/L NiCl2 but not by the T-type Ca(2+) channel blocker mibefradil (300 nmol/L). However, inhibition of Ca(2+) influx via reverse-mode sodium/calcium exchange (NCX) using either 1 μmol/L SEA0400 or 5 μmol/L KB-R7943 did block the effect of high [K(+)]o on ICC. These data suggest that high K(+) solution increases the frequency of calcium waves in ICC by increasing Ca(2+) influx through reverse-mode NCX.

摘要

Cajal间质细胞(ICC)在兔尿道中充当假定的起搏细胞。ICC中的起搏活动源于自发的全局Ca(2+)波,通过提高细胞外[K(+)]可增加其频率。本研究的目的是阐明这种反应的机制。使用Nipkow旋转盘共聚焦显微镜测量用fluo-4负载的平滑肌细胞(SMC)和ICC中的细胞内[Ca(2+)]。将[K(+)]o增加到60 mmol/L会导致[Ca(2+)]i增加,并伴随SMC收缩。提高[K(+)]o不会引起ICC收缩,但自发钙波的发放频率增加。将[Ca(2+)]o降低到0 mmol/L可消除两种细胞类型的反应。1 μmol/L的硝苯地平可阻断SMC对高[K(+)]o的反应,但不影响ICC发放频率的增加。后一种效应可被30 μmol/L的NiCl2阻断,但不能被T型Ca(2+)通道阻滞剂米贝地尔(300 nmol/L)阻断。然而,使用1 μmol/L的SEA0400或5 μmol/L的KB-R7943抑制通过反向模式钠/钙交换(NCX)的Ca(2+)内流确实可阻断高[K(+)]o对ICC的作用。这些数据表明,高钾溶液通过增加通过反向模式NCX的Ca(2+)内流来增加ICC中钙波的频率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3081/3967686/fe61b27ed946/phy2-2-e00203-g1.jpg

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