Nicotine regulates large conductance ca2+ activated K+ channels in rat coronary arterial smooth muscle cells / 中国应用生理学杂志
Chinese Journal of Applied Physiology
; (6): 24-27, 2012.
Article
в Zh
| WPRIM
| ID: wpr-329955
Ответственная библиотека:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>The present study was to explore signaling mechanisms underlying nicotine-induced inhibition of large-conductance calcium-activated potassium channels (BK(Ca)).</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>This phenomenon may serve as a physiological mechanism that nicotine inhibits BK(Ca) channel activity to increase via cAMP/PKA-dependent pathway.</p>
Полный текст:
1
База данных:
WPRIM
Основная тема:
Pharmacology
/
Arteries
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Signal Transduction
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Rats, Wistar
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Patch-Clamp Techniques
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Coronary Vessels
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Cell Biology
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Myocytes, Smooth Muscle
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Large-Conductance Calcium-Activated Potassium Channels
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Metabolism
Пределы темы:
Animals
Язык:
Zh
Журнал:
Chinese Journal of Applied Physiology
Год:
2012
Тип:
Article