Figure 3.

Tonic release of ATP from glial cells generates tone in retinal vessels. Vascular tone is monitored by measuring the diameter of primary retinal arterioles in vivo. (a) Altering endogenous ATP levels changes vascular tone. Intravitreal injection of apyrase, which hydrolyses ATP and lowers ATP levels, dilates vessels. Injection of AOPCP, which prevents normal ATP hydrolysis and raises ATP levels, constricts vessels. Injection of vehicle (saline) in this and other panels, evokes a transient dilation (an artefact of the injection) but little sustained change in diameter. (b) Injection of the ATP analogue ATPγS onto the retinal surface constricts vessels. The delayed vessel dilation is probably owing to ATPγS stimulation of vascular endothelial cells. (c) ATP acts on P2X purinergic receptors to generate vessel tone. Injection of the non-selective purinergic antagonist suramin, the P2X antagonist isoPPADS, the P2X1, P2X2/3 and P2X3 antagonist TNP-ATP and the selective P2X1 antagonist NF023 all dilate retinal vessels. The P2X7 antagonist A438079 has no sustained effect on vessel tone. (d) Glial cells are a source of the vasoconstricting ATP. Injection of the selective gliotoxin fluorocitrate, which blocks ATP production in glial cells, dilates retinal vessels. All panels from Kur & Newman [13].