Abstract
Retinal tissue from different species continuously releases an as yet unidentified retinal relaxing factor (RRF) lowering tone of isolated arteries. The potential influence of adenosine on this relaxing influence was investigated using isometric tension recording of different isolated arteries. The presence of bovine retinal tissue or rat retinal tissue enhanced the vasorelaxing effect of adenosine on isolated bovine retinal artery. In isolated rat carotid artery adenosine elicited no relaxation. However, a small relaxation is observed in the presence of rat retinal tissue, but not in the presence of porcine retina. The fact that adenosine potentiates the effect of rat retinal tissue but not that of a similar piece of porcine retinal tissue indicates species differences. Neither a NO-synthase inhibitor (nitro- l-arginine, 0.1 mM), a cyclooxygenase inhibitor (indomethacin, 10 μM) or an epoxygenase inhibitor (miconazole, 10 μM) influenced the enhanced vasodilating effect of adenosine on bovine retinal arteries in the presence of bovine retinal tissue. On the other hand, when the retinal arteries were contracted with 120 mM K +, adenosine no longer induced relaxation of the preparation with bovine retinal tissue. This is in line with the concept that adenosine enhances the influence of RRF. Also, the fact that rat carotid artery is less sensitive to RRF than bovine retinal artery – corresponding with a less enhanced adenosine response in rat carotid artery – is in line with the potential involvement of the RRF in the enhanced adenosine response. However, experiments using a bioassay setup for RRF gave no evidence for an increased RRF-release from the retina, nor for an increased RRF-sensitivity of the retinal artery in the presence of adenosine. In conclusion, our findings indicate that adenosine potentiates the relaxing influence of bovine and rat retinal tissue. This effect is species dependent as it is not seen with porcine retinal tissue. Neither NO, cyclooxygenase metabolites or epoxyeicosatrienoic acids seem to be involved in this enhanced vasorelaxing response. The involvement of the RRF cannot be excluded.
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