Adenosine decreases permeability of in vitro endothelial monolayers.

The addition of adenosine to perfusates flowing through an in vitro cell-column model of the vasculature decreases the permeability of cell column fetal bovine aortic endothelial monolayers. At 10(-4) M adenosine, cell monolayer permeability to the paracellular tracers polyethylene glycol (mol wt 900) and cyanocobalamin (mol wt 1,355) is significantly decreased within 15 min. In continuous treatments with adenosine for up to 30 min, the permeability reduction is maintained, and removal of adenosine returns permeability to baseline levels within 15 min. The effect of adenosine is concentration dependent, with a 5% reduction in permeability with 10(-6) M adenosine, a 21% reduction with 10(-5) M adenosine, and a 37% reduction with 10(-4) M adenosine. The effects of adenosine are not blocked by the adenosine transport inhibitor dipyridamole. Permeability is significantly reduced by the A2-specific adenosine analogue 5'-(N-cyclopropyl)-carboxamidoadenosine but not by the A1-specific adenosine analogue N6-(L-2-phenylisopropyl)adenosine. In addition, the permeability decrease is blocked by the A2-receptor antagonist 8-phenyltheophylline (10(-5)M). We conclude that adenosine decreases the permeability of bovine fetal aortic endothelial monolayers via endothelial A2-purinoceptors.