Ca2+ Flux Through Voltage-Gated Channels with Flow Cessation in Pulmonary Microvascular Endothelial Cells
Z Wei, Y Manevich, AB Al-Mehdi, S Chatterjee… - …, 2004 - Taylor & Francis
Z Wei, Y Manevich, AB Al-Mehdi, S Chatterjee, AB Fisher
Microcirculation, 2004•Taylor & FrancisObjective: 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 …
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 …
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.
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