AI Article Synopsis
- The study examines how voltage-gated Ca2+ channels contribute to calcium ion influx when blood flow stops in specific rat endothelial cells.
- Researchers measured the levels of Ca2+ channels and their activity using inhibitors while tracking real-time changes in calcium influx and cell membrane potential.
- Findings reveal that T-type Ca2+ channels are upregulated in response to flow and play a key role in calcium influx during moments of flow cessation, linked to membrane depolarization.
Article 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.
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| http://dx.doi.org/10.1080/10739680490476367 | DOI Listing |
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