Related Experiment Videos
Endothelial cell shrinkage increases permeability through a Ca2+-dependent pathway in single frog mesenteric
1Department of Human Physiology, School of Medicine, University of California, Davis, CA 95616, USA.
The Journal of Physiology
|June 22, 1999
Summary
Calcium influx into endothelial cells is essential for increased microvessel permeability when endothelial cell-extracellular matrix attachments are disrupted by hypertonic solutions.
Area of Science:
- Physiology
- Cell Biology
- Microcirculation Research
Background:
- Endothelial cell (EC)-extracellular matrix (ECM) attachment influences microvessel hydraulic permeability (Lp).
- Hypertonic solutions can alter EC-ECM attachment and increase Lp.
- Calcium (Ca2+) dependent mechanisms' role in this process was previously unclear.
Purpose of the Study:
- To determine if Ca2+-dependent mechanisms are essential for the observed increase in microvessel Lp.
- To investigate the role of Ca2+ influx in response to hypertonic solutions when EC-ECM attachments are disrupted.
Main Methods:
- Experiments were conducted on single perfused mesenteric microvessels in pithed frogs (Rana pipiens).
- EC-ECM attachments were disrupted using Gly-Arg-Gly-Asp-Thr-Pro (GRGDTP).
- Ca2+ influx was reduced using high K+ solutions to depolarize the endothelial membrane.
Main Results:
- Disrupting EC-ECM attachments with GRGDTP and exposing microvessels to hypertonic solutions normally increases Lp.
- High K+ solutions, which reduce Ca2+ influx, abolished the Lp increase caused by hypertonic solutions in GRGDTP-treated microvessels.
- This effect was dose-dependent, with higher K+ concentrations more effectively attenuating the Lp increase.
Conclusions:
- Ca2+ entry into endothelial cells via passive conductance channels is necessary for the increase in microvessel Lp.
- This Ca2+ influx is critical when EC-ECM attachments are compromised, particularly under hypertonic stress.