Abstract
Purpose:
To investigate the vasomotor activity of prostacyclin (PGI2) on porcine retinal arterioles.
Methods:
Porcine retinal arterioles were isolated, cannulated, and pressurized without flow in vitro. Changes in diameter were recorded using videomicroscopic techniques. To confirm the role of the endothelium, we compared the responses before and after endothelial removal. To examine the involvement of endothelium-derived relaxing factor nitric oxide (NO), we assessed the responses in the presence of NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME).
Results:
The retinal arterioles dilated in a concentration-dependent manner in response to PGI2. This vasodilation decreased significantly after the endothelium was removed. L-NAME significantly inhibited PGI2-induced vasodilation comparable to denudation.
Conclusions:
PGI2 elicits vasodilation of the retinal arterioles mediated not only by the vascular smooth muscle but also the endothelium, suggesting that an endothelium-dependent component of PGI2-induced vasodilation may be involved because of production of NO. We speculated that cross-talk between NO and PGI2 may exist in the retinal circulation.
Keywords: 436 blood supply •
688 retina •
749 vascular occlusion/vascular occlusive disease