Received December 2, 2003
Revised January 6, 2004
Accepted after revision February 18, 2004
The role of endothelial cell Ca2+ store release in the regulation of Rana microvascular permeability in vivo
Catherine A Glass 1
David O Bates 1*
1 University of Bristol
* To whom correspondence should be addressed. E-mail: dave.bates{at}bris.ac.uk.
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Abstract |
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Microvascular permeability is regulated by changes in intracellular calcium concentration. The mechanism by which this increase in calcium determines permeability under normal conditions and during stimulation with agonists remains to be elucidated. In order to determine whether calcium release from intracellular stores could contribute towards the regulation of vascular permeability, hydraulic conductivity (Lp) was measured in frog mesenteric microvessels during stimulation of the endothelial cells of those vessels with agonists that release calcium from these stores. ATP (which acts through activation of IP3 receptors) increased Lp in the absence of calcium influx across the plasma membrane 2.3±0.3 fold (mean ± sem, p<0.01 n=8), which was less than the increase in the presence of calcium influx (3.1±1.1 fold). Caffeine (which acts through activation of ryanodine receptors) also increased Lp in the absence of calcium influx across the plasma membrane 3.8±1.0 fold (p<0.01 n=9), but by at least as much as it does with calcium influx (2.8±0.5 fold). Surprisingly, there was a strong positive correlation between the size of the response during store release and the baseline permeability (r=0.91 for ATP, r=0.75 for caffeine). This suggests that the filling state of the stores may regulate the baseline permeability of the microvessels.
Key Words:
Calcium store, Microcirculation, Permeability
