Cultured canine jugular vein endothelial cells were seeded on polycarb
onate filters to create an in vitro permeability assay. The calculated
diffusive permeability coefficient for FITC-BSA across untreated mono
layers was 1.1 +/- 0.4 X 10(-6) cm/s. After 15-min incubations with ei
ther histamine or bradykinin, the resistance to albumin flux across th
e monolayers was reduced significantly. Diffusive albumin permeability
coefficients were 3.4 +/- 1.8 X 10(-6) and 4.1 +/- 2.0 X 10(-6) cm/s,
respectively. Ultrastructural morphometric analyses of the endothelia
l cell monolayers served to define uniform dimensions of intercellular
clefts and similar plasmalemmal vesicle densities in the untreated an
d the vasomediator-activated monolayers. These results are consistent
with the interpretation that the vasomediator-activated pathway across
the venous endothelial monolayers is not dependent on sustained inter
cellular gap formation or sustained expansion of the plasmalemmal vesi
cle population for the 15-min observation periods. Whether the increas
ed albumin flux is dependent on transient gap formation or on physical
changes within the venous endothelial cell glycocalyx remains to be t
ested.