title: Ca2+ flux through voltage-gated channels with flow cessation in pulmonary microvascular endothelial cells.
abstract: OBJECTIVE
  To investigate the role of voltage-gated Ca2+ channels in Ca2+ influx with flow cessation in flow-adapted rat pulmonary microvascular endothelial cells.
  
  
  METHODS
  Cells were evaluated for mRNA and protein levels for major components of the voltage-gated Ca2+ channels. Ca2+ influx with flow cessation and cell membrane potential were measured in real time with fluorescent dyes. Mibefradil and nifedipine were used as inhibitors of Ca2+ channel activity.
  
  
  RESULTS
  Voltage-gated Ca2+ channel protein and mRNA for the T-type channel were expressed at a relatively low level in endothelial cells cultured under static conditions and expression was induced significantly during flow adaptation. Flow-adapted but not control cells showed Ca2+ influx during flow cessation that was blocked by mibefradil but not by nifedipine. Ca2+ influx also was blocked by cromakalim, a KATP channel agonist. Cell membrane depolarization with flow cessation was unaffected by mibefradil.
  
  
  CONCLUSIONS
  Rat pulmonary microvascular endothelial cells express T-type voltage-gated Ca2+ channels that are induced during adaptation to flow and are responsible for Ca2+ influx that occurs as a result of flow cessation-mediated membrane depolarization.
authors.affiliation: Institute for Environmental Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, USA.
authors.forename: Zhihua
authors.initials: Z
authors.lastname: Wei
authors.forename: Yefim
authors.initials: Y
authors.lastname: Manevich
authors.forename: Abu B
authors.initials: AB
authors.lastname: Al-Mehdi
authors.forename: Shampa
authors.initials: S
authors.lastname: Chatterjee
authors.forename: Aron B
authors.initials: AB
authors.lastname: Fisher
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020747:Calcium Channels, T-Type / Q000235:genetics / Q000378:metabolism*; D002196:Capillaries / Q000166:cytology; D019806:Cromakalim / Q000494:pharmacology; D042783:Endothelial Cells / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D015640:Ion Channel Gating / Q000187:drug effects; D017136:Ion Transport / Q000187:drug effects*; D008168:Lung / Q000098:blood supply*; D008564:Membrane Potentials / Q000187:drug effects; D020748:Mibefradil / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012212:Rheology
chemical_list: D002121:Calcium Channel Blockers; D020747:Calcium Channels, T-Type; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D012333:RNA, Messenger; D019806:Cromakalim; D020748:Mibefradil; D009543:Nifedipine; D002118:Calcium