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Related Experiment Videos

Asynchronous Ca(2+) waves in intact venous smooth muscle.

D O Ruehlmann1, C H Lee, D Poburko

  • 1Vancouver Vascular Biology Research Centre, University of British Columbia, St. Paul's Hospital, Vancouver, BC, Canada.

Circulation Research
|March 4, 2000
PubMed
Summary

Caffeine and phenylephrine (PE) trigger calcium waves in rabbit inferior vena cava smooth muscle cells. Asynchronous calcium oscillations in these cells explain whole-tissue contraction, with PE enhancing oscillation frequency.

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Area of Science:

  • Cardiovascular Physiology
  • Cellular Biology
  • Smooth Muscle Pharmacology

Background:

  • The rabbit inferior vena cava (IVC) is a significant capacitance vessel.
  • Vascular smooth muscle cells (VSMCs) exhibit contractile responses to various stimuli.
  • Understanding the subcellular mechanisms of contraction is crucial for cardiovascular research.

Purpose of the Study:

  • To correlate whole-tissue contractile responses of the IVC with intracellular calcium ([Ca(2+)](i)) signaling in VSMCs.
  • To investigate the mechanisms of calcium wave propagation and oscillation in response to caffeine and phenylephrine (PE).
  • To elucidate the relationship between VSMC calcium dynamics and overall vascular contractility.

Main Methods:

  • Experiments were conducted on endothelium-denuded rabbit IVC segments.

Related Experiment Videos

  • Confocal microscopy was used to visualize subcellular [Ca(2+)](i) signals in situ.
  • Contractile responses were measured alongside [Ca(2+)](i) dynamics in response to varying concentrations of caffeine and PE.
  • Pharmacological agents like ryanodine were used to probe calcium release mechanisms.

    • Main Results:

    • Both caffeine and PE induced initial Ca(2+) waves in individual VSMCs.
    • Caffeine-induced Ca(2+) signals returned to baseline, while PE caused repetitive, asynchronous Ca(2+) waves (oscillations).
    • These oscillations were sensitive to ryanodine and caffeine, indicating sarcoplasmic reticulum involvement.
    • The lack of synchronicity in VSMC Ca(2+) oscillations correlated with tonic whole-tissue contraction.
    • Caffeine-induced contraction depended on the recruitment of VSMCs with varying sensitivities.
    • PE enhanced the frequency of asynchronous Ca(2+) oscillations in recruited VSMCs.

    Conclusions:

    • Asynchronous Ca(2+) oscillations in VSMCs are a key mechanism underlying tonic contraction in the IVC.
    • Caffeine and PE activate VSMCs through distinct but related calcium signaling pathways.
    • Differential recruitment of VSMCs and enhanced oscillation frequency by PE contribute to its dose-dependent contractile effects.