Nicorandil stimulates a Na+/Ca2+ exchanger by activating guanylate cyclase in guinea pig cardiac myocytes

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• 作者：Jiazhang Wei ; Yasuhide Watanabe…
• 关键词：Nicorandil ; KATP channel opener ; Na+/Ca2+ exchange current (I NCX) ; Cardiac myocytes ; Cyclic GMP
• 刊名：Pfl¨¹gers Archiv - European Journal of Physiology
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：468
• 期：4
• 页码：693-703
• 全文大小：1,037 KB
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• 作者单位：Jiazhang Wei (1)
  Yasuhide Watanabe (2)
  Kazuhiko Takeuchi (1)
  Kanna Yamashita (2)
  Miyuki Tashiro (2)
  Satomi Kita (3)
  Takahiro Iwamoto (3)
  Hiroshi Watanabe (1)
  Junko Kimura (4)
  
  1. Department of Clinical Pharmacology and Therapeutics, Hamamatsu University School of Medicine, Hamamatsu, 431-3192, Japan
  2. Division of Pharmacological Science, Department of Health Science, Hamamatsu University School of Medicine, Hamamatsu, 431-3192, Japan
  3. Department of Pharmacology, Faculty of Medicine, Fukuoka University, Fukuoka, 814-0180, Japan
  4. Department of Pharmacology, Fukushima Medical University, Fukushima, 960-1295, Japan
  
• 刊物主题：Human Physiology;
• 出版者：Springer Berlin Heidelberg
• ISSN：1432-2013

文摘

Nicorandil, a hybrid of an ATP-sensitive K+ (KATP) channel opener and a nitrate generator, is used clinically for the treatment of angina pectoris. This agent has been reported to exert antiarrhythmic actions by abolishing both triggered activity and spontaneous automaticity in an in vitro study. It is well known that delayed afterdepolarizations (DADs) are caused by the Na+/Ca2+ exchange current (I _NCX). In this study, we investigated the effect of nicorandil on the cardiac Na+/Ca2+ exchanger (NCX1). We used the whole-cell patch clamp technique and the Fura-2/AM (Ca2+ indicator) method to investigate the effect of nicorandil on I _NCX in isolated guinea pig ventricular myocytes and CCL39 fibroblast cells transfected with dog heart NCX1. Nicorandil enhanced I _NCX in a concentration-dependent manner. The EC₅₀ (half-maximum concentration for enhancement of the drug) values were 15.0 and 8.7 μM for the outward and inward components of I _NCX, respectively. 8-Bromoguanosine 3′,5′-cyclic monophosphate (8-Br-cGMP), a membrane-permeable analog of guanosine 3′,5′-cyclic monophosphate (cGMP), enhanced I _NCX. 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor (10 μM), completely abolished the nicorandil-induced I _NCX increase. Nicorandil increased I _NCX in CCL39 cells expressing wild-type NCX1 but did not affect mutant NCX1 without a long intracellular loop between transmembrane segments (TMSs) 5 and 6. Nicorandil at 100 μM abolished DADs induced by electrical stimulation with ouabain. Nicorandil enhanced the function of NCX1 via guanylate cyclase and thus may accelerate Ca2+ exit via NCX1. This may partially contribute to the cardioprotection by nicorandil in addition to shortening action potential duration (APD) by activating KATP channels.