Lack of effect of Z-butylidenephthalide on presynaptic N-type Ca2+ channels in isolated guinea-pig ileum

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• 作者：Marcelo Chen ; Wun-Chang Ko
• 关键词：Acetylcholine ; Z ; Butylidenephthalide ; ω ; Conotoxin GVIA ; Nifedipine ; Electrically induced twitch response ; Guinea ; pig ileum
• 刊名：Naunyn-Schmiedeberg's Archives of Pharmacology
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：389
• 期：2
• 页码：159-166
• 全文大小：720 KB
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• 作者单位：Marcelo Chen (1) (2)
  Wun-Chang Ko (3)
  
  1. Department of Urology, Mackay Memorial Hospital, Taipei, Taiwan
  2. Department of Cosmetic Application and Management, Mackay Junior College of Medicine, Nursing and Management, Taipei, Taiwan
  3. Department of Pharmacology, College of Medicine, Taipei Medical University, 250 Wu-Hsing St, Taipei, 110, Taiwan
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Pharmacology and Toxicology
  Neurosciences
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-1912

文摘

Z-Butylidenephthalide (Bdph) was reported to more potently inhibit electrically induced twitch responses than acetylcholine-induced tonic contraction in isolated guinea-pig ileum (GPI). The aim of the present study was to investigate the inhibitory effects of Z-Bdph on Ca2+ and K+ channels on GPI. In Locke-Ringer’s solution, both responses were isometrically recorded on a polygraph. Incubation of ω-conotoxin MVIIC, but not Z-Bdph, in the electrically stimulated GPI prior to adding ω-conotoxin GVIA, an irreversible blocker of N-type voltage-dependent Ca2+ channels (VDCCs), protected the binding sites and resulted in the twitch responses reversible by washing, suggesting that Z-Bdph did not bind to the N-type VDCCs. Interestingly, we found Z-Bdph concentration dependently delayed the onsets of K+-induced twitch responses, suggesting that Z-Bdph may be a blocker of K+ channels to interfere extracellular K+ across through the pre-junctional membrane of nerve ending in K+-free medium. Z-Bdph similar to nifedipine non-competitively inhibited cumulative ACh-induced phasic contractions, suggesting that Z-Bdph may bind to L-type of inositol-1,4,5-trisphosphate (IP₃)-sensitive Ca2+ channels on the endoplasmic reticulum (ER) membrane. In the presence of verapamil, a L-type Ca2+ channel blocker or Z-Bdph, the twitch inhibitions by either were effectively reversed by exogenous Ca2+, suggesting that they may freely pass through pre-junctional N-type, but not L-type which was blocked at least a part by either, of VDDCs open when each electrical coaxial stimulation (ECS) into intracellular space of cholinergic nerve terminal and trigger release of transmitters. In conclusion, results confirm that Z-Bdph more potently inhibits ECS-induced twitch responses than ACh-induced PCs in GPI and suggest that this effect is not mediated by interaction with presynaptic N-type VDCCs.