Nicotine regulates large conductance ca2+ activated K+ channels in rat coronary arterial smooth muscle cells.
- Author:
Xiang-Quan KONG
1
;
Yu-Wen YANG
;
Jing-Han JIANG
;
Hui ZHANG
;
Qian LI
;
Wei-Hua WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Arteries; cytology; drug effects; metabolism; Coronary Vessels; cytology; drug effects; metabolism; Large-Conductance Calcium-Activated Potassium Channels; metabolism; Male; Myocytes, Smooth Muscle; drug effects; metabolism; Nicotine; pharmacology; Patch-Clamp Techniques; Rats; Rats, Wistar; Signal Transduction
- From: Chinese Journal of Applied Physiology 2012;28(1):24-27
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEThe present study was to explore signaling mechanisms underlying nicotine-induced inhibition of large-conductance calcium-activated potassium channels (BK(Ca)).
METHODS8 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.
RESULTSCPT-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.
CONCLUSIONThis phenomenon may serve as a physiological mechanism that nicotine inhibits BK(Ca) channel activity to increase via cAMP/PKA-dependent pathway.
