Pacemaker activity in urethral interstitial cells is not dependent on capacitative calcium entry
Pacemaker activity in urethral interstitial cells is not dependent on capacitative calcium entry
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DOI：
10.1152/ajpcell.00090.2005
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发表时间：
2005-09-01
影响因子：
5.5
通讯作者：
Sergeant, GP
中科院分区：
文献类型：
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作者：
Bradley, E;Hollywood, MA;Sergeant, GP
本研究旨在探讨兔尿道间质细胞（IC）中容性Ca2+进入（CCE）的性质和作用。与对照组相比，在细胞内Ca2+储存耗尽的细胞中，IC中的Ca2+进入量更大，这与通过CCE途径的内流一致。非选择性Ca2+进入阻断剂Gd3+ (10 μ M)、La3+ (10 μ M)和Ni2+ (100 μ M)分别使CCE降低67% （n = 14）、65% （n = 11）和55% （n = 9）。当储存未耗尽时，这些药物不抑制Ca2+进入。相反，IC中的CCE对SKF-96365 （10 μ M）、wortmannin （10 μ M）和硝苯地平（1 μ M）耐药。从箝位在-60 mV的IC中记录了自发瞬态内向电流。Gd3+ (10 μ M)或La3+ (10 μ M)对这些事件的影响不显著，仅在100 μ M Ni2+的作用下幅度略有下降。本研究结果表明，兔尿道新鲜分散的IC具有CCE通路。然而，通过这一途径的内流似乎并不能促进这些细胞的自发活动。
The aim of the present study was to investigate the properties and role of capacitative Ca2+ entry (CCE) in interstitial cells (IC) isolated from the rabbit urethra. Ca2+ entry in IC was larger in cells with depleted intracellular Ca2+ stores compared with controls, consistent with influx via a CCE pathway. The nonselective Ca2+ entry blockers Gd3+ ( 10 mu M), La3+ (10 mu M), and Ni2+ ( 100 mu M) reduced CCE by 67% (n = 14), 65% (n = 11), and 55% ( n = 9), respectively. These agents did not inhibit Ca2+ entry when stores were not depleted. Conversely, CCE in IC was resistant to SKF-96365 ( 10 mu M), wortmannin ( 10 mu M), and nifedipine ( 1 mu M). Spontaneous transient inward currents were recorded from IC voltage-clamped at -60 mV. These events were not significantly affected by Gd3+ (10 mu M) or La3+ ( 10 mu M) and were only slightly decreased in amplitude by 100 mu M Ni2+. The results from this study demonstrate that freshly dispersed IC from the rabbit urethra possess a CCE pathway. However, influx via this pathway does not appear to contribute to spontaneous activity in these cells.