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Related Experiment Videos

Ca2+ entry through conductive pathway modulates receptor-mediated increase in microvessel permeability

P He1, X Zhang, F E Curry

  • 1Department of Human Physiology, School of Medicine, University of California, Davis 95616, USA.

The American Journal of Physiology
|December 1, 1996
PubMed
Summary

Calcium influx into endothelial cells is essential for increased microvessel permeability during inflammation. This study shows Ca2+ entry is required for venular microvessel responses to inflammatory agents.

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Area of Science:

  • Physiology
  • Cell Biology
  • Microcirculation Research

Background:

  • Receptor-mediated signaling often involves changes in intracellular calcium.
  • Microvessel permeability is crucial for regulating fluid and solute exchange.
  • Inflammatory mediators can alter microvessel barrier function.

Purpose of the Study:

  • To investigate the role of cytoplasmic calcium concentration ([Ca2+]i) in receptor-mediated increases in microvessel permeability.
  • To determine if calcium entry into endothelial cells is required for acute increases in venular microvessel permeability.
  • To characterize the properties of the calcium entry pathway.

Main Methods:

  • Perfusing isolated frog and hamster venular microvessels.
  • Stimulating microvessels with ATP, high-K+ Ringer solution, Ca2+ ionophores, bradykinin, and histamine.

Related Experiment Videos

  • Measuring cytoplasmic Ca2+ concentration ([Ca2+]i) using fluorescence indicators.
  • Assessing microvessel hydraulic conductivity (Lp) as a measure of permeability.

    • Main Results:

    • ATP exposure increased [Ca2+]i and hydraulic conductivity (Lp) in frog microvessels.
    • Removal of extracellular Ca2+ abolished significant Lp increase and attenuated [Ca2+]i rise.
    • High-K+ depolarization reduced the [Ca2+]i and Lp increases.
    • Evidence suggests a passive conductance pathway for Ca2+ entry into endothelial cells.

    Conclusions:

    • Ca2+ entry into endothelial cells is necessary for the acute increase in venular microvessel permeability induced by inflammatory agents.
    • The identified Ca2+ entry pathway exhibits characteristics of passive conductance.
    • Similar mechanisms are implicated in both frog and hamster microvessels, suggesting conserved pathways for permeability regulation.