Article

[Nicotine regulates large conductance ca2+ activated K+ channels in rat coronary arterial smooth muscle cells].

Yijishan Hospital of Wannan Medical School, Wuhu 241001, China.
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 01/2012; 28(1):24-7. pp.24-7
Source: PubMed

ABSTRACT The present study was to explore signaling mechanisums underlying nicotine-induced inhibition of large-conductance calcium-activated potassium channels (BK(Ca)).
8 week male Wistar rats were divided randomly into saline group and nicotine group and received respectively injection with saline or nicotine (Sigma, Shanghai, China) at 2 mg/(kg x d) for 21 days. Coronary vascular smooth muscle cells were dissociated enzymatically. Dissociated smooth muscle cells were interfered with CPT-cAMP (100 micromol/L) or forskolin (10 micromol/L). The signal channel open dwell-time (To), close dwell-time (Tc) and open probability (Po) were recorded.
CPT-cAMP or forskolin significantly prolonged To, shorten Tc and increased Po in saline group (P < 0.01). But in nicotine group To, Tc and Po did not been changed.
This phenomenon may serve as a physiological mechanism that nicotine inhibits BK(Ca) channel activity to increase via cAMP/PKA-dependent pathway.

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Keywords

10 micromol/L
 
8 week male Wistar rats
 
cAMP/PKA-dependent pathway
 
Coronary vascular smooth muscle cells
 
CPT-cAMP
 
Dissociated smooth muscle cells
 
forskolin
 
large-conductance calcium-activated potassium channels
 
nicotine inhibits BK(Ca)
 
nicotine-induced inhibition
 
open probability
 
physiological mechanism
 
randomly
 
saline
 
saline group
 
signal channel open dwell-time
 
signaling mechanisums