Propofol Causes Sustained Ca2+Elevation in Endothelial Cells by Stimulating Ryanodine Receptor and Suppressing Plasmalemmal Ca2+Pump

Chin Min Chuang, Cing Yu Chen, Pao Sheng Yen, Cheng Hsun Wu, Lian Ru Shiao, Kar Lok Wong, Paul Chan, Yuk Man Leung

研究成果: 雜誌貢獻文章同行評審

1 引文 斯高帕斯(Scopus)

摘要

Propofol, a general anesthetic administered intravenously, may cause pain at the injection site. The pain is in part due to irritation of vascular endothelial cells. We here investigated the effects of propofol on Ca2+transport and pain mediator release in human umbilical vein endothelial cells (EA.hy926). Propofol mobilized Ca2+from cyclopiazonic acid (CPA)-dischargeable pool but did not cause Ca2+release from the lysosomal Ca2+stores. Propofol-elicited Ca2+release was suppressed by 100 M ryanodine, suggesting the participation of ryanodine receptor channels. Propofol did not affect ATP-triggered Ca2+release but abolished the Ca2+influx triggered by ATP; in addition, propofol also suppressed store-operated Ca2+entry elicited by CPA. Ca2+clearance during CPA-induced Ca2+discharge was unaffected by a low Na+(50 mM) extracellular solution, but strongly suppressed by 5 mM La3+(an inhibitor of plasmalemmal Ca2+pump), suggesting Ca2+extrusion was predominantly through the plasmalemmal Ca2+pump. Propofol mimicked the effect of La3+in suppressing Ca2+clearance. Propofol also stimulated release of pain mediators, namely, reactive oxygen species and bradykinin. Our data suggest propofol elicited Ca2+release and repressed Ca2+clearance, causing a sustained cytosolic [Ca2+]i elevation. The latter may cause reactive oxygen species and bradykinin release, resulting in pain.
原文英語
頁(從 - 到)749-757
頁數9
期刊Journal of Cardiovascular Pharmacology
79
發行號5
DOIs
出版狀態已發佈 - 5月 25 2022

ASJC Scopus subject areas

  • 藥理
  • 心臟病學與心血管醫學

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