Calcium entry through conductive pathway modulates receptor
-mediated increase in microvessel permeability.
He, P., X. Zhang, and F. E. Curry.
Department of Human Physiology, School of Medicine, University of
California, Davis, CA 95616
APStracts 3:0225H, 1996.
We investigated the relationship between receptor mediated increases
in cytoplasmic calcium concentration [Ca2+]i, and increased
microvessel permeability. In individually perfused venular
microvessels of frog mesentery exposed to 10 mM ATP, [Ca2+]i
increased from 59 7 nM to 172 21 nM within 1 minute, then fell back
towards control values. The corresponding peak increase in the
hydraulic conductivity of the microvessel wall (Lp) was 5.7 0.5 fold
relative to control. After removal of extracellular calcium, there
was no significant increase in Lp and the initial increase in [Ca2+]i
was attenuated, but not abolished. Depolarization of the endothelial
cell membrane with high potassium Ringer's solution reduced the peak
increase in [Ca2+]i to 106 7 nM, and attenuated the increase in Lp to
1.8 0.4 fold. The results conform to the hypothesis that calcium ion
entry into endothelial cells is required for acute increase in
venular microvessel permeability by inflammatory agents, and that the
pathway for calcium entry has the properties of a passive conductance
pathway. Similar conclusions were reached in previous experiments in
frog microvessels exposed to calcium ionophores and perfusates with
no plasma proteins. In venular microvessels of hamster mesentery
exposed to ATP and bradykinin, a similar pathway for calcium entry
was demonstrated in the present experiments. We did not measure
permeability changes in hamster microvessels in this study, but these
microvessels respond to histamine and ionophores with a transient
increase in permeability to macromolecules similar to that measured
in frog microvessels (Am. J. Physiol. 268: H1982-1991, 1995).
Received 9 November 1995; accepted in final form 22 May 1996.
APS Manuscript Number H1053-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 June 96