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Related Experiment Videos

Capacitative Ca(2+) entry in agonist-induced pulmonary vasoconstriction.

S S McDaniel1, O Platoshyn, J Wang

  • 1Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California School of Medicine, San Diego, California 92103, USA.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|April 6, 2001
PubMed
Summary

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Capacitative calcium entry (CCE) in pulmonary artery smooth muscle cells is crucial for sustained contractions. This process, potentially mediated by transient receptor potential channels, is vital for regulating vascular tone.

Area of Science:

  • Physiology
  • Pharmacology
  • Cell Biology

Background:

  • Agonist stimulation causes cytosolic calcium increases in pulmonary artery smooth muscle cells via intracellular store release and sustained influx.
  • Capacitative calcium entry (CCE) is triggered by depleted intracellular calcium stores, sustaining elevated cytosolic calcium and refilling stores.

Purpose of the Study:

  • To investigate the role of CCE in phenylephrine-induced pulmonary artery smooth muscle cell contraction.
  • To identify the potential molecular mechanisms, specifically transient receptor potential (TRP) channels, involved in CCE.

Main Methods:

  • Isolated pulmonary arteries were stimulated with phenylephrine in calcium-free solutions.
  • Capacitative calcium entry was assessed upon restoration of extracellular calcium.

Related Experiment Videos

  • The effect of the store-operated calcium channel blocker, Ni(2+), was evaluated.
  • RT-PCR was used to identify TRP gene transcripts in single pulmonary artery smooth muscle cells.

    • Main Results:

    • Phenylephrine induced a transient contraction, followed by store depletion.
    • Restoration of extracellular calcium in the presence of phentolamine caused a CCE-mediated contraction.
    • Ni(2+) inhibited CCE and CCE-mediated contraction.
    • Five TRP gene transcripts were identified in pulmonary artery smooth muscle cells.

    Conclusions:

    • Capacitative calcium entry plays a significant role in agonist-induced pulmonary artery contraction.
    • CCE is potentially mediated by calcium channels encoded by transient receptor potential genes.