Adenosine and its agonists cause retinal vasodilation and hemorrhages. Implications for ischemic retinopathies.

Animals were given a 0.1-mL intravitreous injection of various agents and followed up with frequent ophthalmoscopic examinations. Fundus photographs were performed before injection and at six and 24 hours after injection. Vascular caliber was assessed by a previously described technique of performing measurements on fundus photographs taken and projected in a standardized fashion. No significant vascular dilation was identified for vehicle alone, carbachol, histamine, isoproterenol hydrochloride, or bradykinin. Mild dilation within one hour, but not persisting for 24 hours, was noted for dibutyryl cyclic adenosine monophosphate. Prominent dilation within one hour, becoming maximal by five hours but not persisting for 24 hours, was noted for adenosine, dipyridamole, and sodium nitroprusside. The adenosine-induced vasodilation was effectively blocked by an adenosine receptor antagonist, BW-A1433U. N-ethylcarboxamidoadenosine (NECA), a nonspecific adenosine selective agonist, was a much more potent vasodilator than two relatively selective A1 adenosine agonists, N6-cyclopentyladenosine and N6-phenylisopropyladenosine, suggesting that A2 receptors are involved. The vascular dilation caused by adenosine, dipyridamole, and particularly NECA, but not nitroprusside or dibutyryl cyclic adenosine monophosphate, was accompanied by retinal hemorrhages, producing a picture reminiscent of some features of ischemic retinopathies. This study suggests that adenosine may be an important mediator of vasodilation, and therefore blood flow, in the retina.