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Involvement of the phosphatidylinositol kinase pathway in augmentation of ATP-sensitive K+ channel currents by hypo-osmotic stress in rat ventricular myocytes

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/53391

Title: Involvement of the phosphatidylinositol kinase pathway in augmentation of ATP-sensitive K+ channel currents by hypo-osmotic stress in rat ventricular myocytes
Authors: Mitsuyama, Hirofumi Browse this author
Yokoshiki, Hisashi Browse this author →KAKEN DB
Irie, Yuki Browse this author
Watanabe, Masaya Browse this author
Mizukami, Kazuya Browse this author
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Keywords: hypo-osmotic stress
ATP-sensitive K+ channels
wortmannin
phosphatidylinositol kinases
K+ channel opening drug
cardiomyocytes
Issue Date: Sep-2013
Publisher: Canadian science publishing, nrc research press
Journal Title: Canadian journal of physiology and pharmacology
Volume: 91
Issue: 9
Start Page: 686
End Page: 692
Publisher DOI: 10.1139/cjpp-2012-0408
PMID: 23984989
Abstract: The objective of this study was to investigate the mechanisms of increase in the efficacy of ATP-sensitive K+ channel (K-ATP) openings by hypo-osmotic stress. The whole-cell K-ATP currents (I-K,I-ATP) stimulated by 100 mu mol/L pinacidil, a K+ channel opening drug, were significantly augmented during hypo-osmotic stress (189 mOsmol/L) compared with normal conditions (303 mOsmol/L). The EC50 and E-max value for pinacidil-activated I-K,I-ATP (measured at 0 mV) was 154 mu mol/L and 844 pA, respectively, in normal solution and 16.6 mu mol/L and 1266 pA, respectively, in hypo-osmotic solution. Augmentation of I-K,I-ATP during hypo-osmotic stress was attenuated by wortmannin (50 mu mol/L), an inhibitor of phosphatidylinositol 3- and 4-kinases, but not by (i) phalloidin (30 mu mol/L), an actin filament stabilizer, (ii) the absence of Ca2+ from the internal and external solutions, and (iii) the presence of creatine phosphate (3 mmol/L), which affects creatine kinase regulation of the K-ATP channels. In the single-channel recordings, an inside-out patch was made after approximately 5 min exposure of the myocyte to hypo-osmotic solution. However, the IC50 value for ATP under such conditions was not different from that obtained in normal osmotic solution. In conclusion, hypo-osmotic stress could augment cardiac I-K,I-ATP through intracellular mechanisms involving the phosphatidylinositol kinase pathway.
Relation: http://www.nrcresearchpress.com/journal/cjpp
Type: article (author version)
URI: http://hdl.handle.net/2115/53391
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 横式 尚司

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