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Pacemaking through Ca2+ stores interacting as coupled oscillators via membrane depolarization.

Mohammad S Imtiaz1, Jun Zhao, Kayoko Hosaka

  • 1Neuroscience Group, School of Biomedical Sciences, Faculty of Health, The University of Newcastle, Newcastle, Australia. mohammad.imtiaz@newcastle.edu.au

Biophysical Journal
|March 14, 2007
PubMed
Summary

Lymphatic vasomotion is driven by coupled calcium (Ca2+) release from inositol 1,4,5-trisphosphate receptor (IP3R)-operated stores acting as oscillators. This mechanism underlies pacemaker potentials and smooth muscle contractions in lymphatic vessels.

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Area of Science:

  • Physiology
  • Cell Biology
  • Biophysics

Background:

  • Lymphatic vasomotion is crucial for fluid homeostasis and immune function.
  • The underlying cellular mechanisms of lymphatic pacemaking remain incompletely understood.
  • Inositol 1,4,5-trisphosphate receptor (IP3R)-operated Ca2+ stores are implicated in cellular signaling.

Purpose of the Study:

  • To investigate the role of IP3R-operated Ca2+ stores in lymphatic smooth muscle pacemaking.
  • To test the hypothesis that coupled Ca2+ store oscillators drive lymphatic vasomotion.
  • To elucidate the contribution of Ca2+ signaling and membrane potential to lymphatic contractions.

Main Methods:

  • Application of Endothelin-1 (ET-1) to quiescent lymphatic smooth muscle.
  • Pharmacological blockade of L-type Ca2+ channels with nifedipine.
  • Computational modeling of lymphatic smooth muscle dynamics.
  • Measurement of intracellular Ca2+ transients and membrane potential.

Main Results:

  • ET-1 enhanced spontaneous Ca2+ transients and waves, leading to global synchronous Ca2+ transients, action potentials, and vasomotion.
  • Nifedipine abolished ET-1-induced synchronous Ca2+ transients and action potentials, leaving only local Ca2+ waves.
  • A computational model incorporating oscillatory Ca2+ release, L-type Ca2+ channels, and gap junctions accurately simulated the experimental data.
  • Coupled oscillator-based interactions of Ca2+ stores, strongly coupled by membrane potential, were identified as the core pacemaking mechanism.

Conclusions:

  • Lymphatic pacemaking is mediated by coupled oscillator-based interactions between active Ca2+ stores.
  • Membrane potential provides strong electrochemical coupling between Ca2+ store oscillators, driving vasomotion.
  • This Ca2+ store-based pacemaking mechanism is likely relevant to various excitable cell types, including gastrointestinal, urethral, vascular, and cardiac tissues.