Retinal tissue modulates retinal arterial tone through the release of a potent vasodilating factor

Various intercellular messenger molecules, such as nitric oxide, adenosine and prostanoids, released by perivascular tissue have been implicated in the control of local blood flow. The present work performed in vitro on isolated retinal arteries advances that perivascular retinal tissue releases yet another intercellular messenger molecule exerting a potent vasodilatory influence. In these experiments, isolated bovine retinal arteries (mounted in a wire-myograph) incompletely cleaned of retinal tissue contracted weaker in response to prostaglandin F2 alpha, than arteries without retinal tissue. This also applied for thromboxane-, endothelin-, and serotonin-induced contractions. Apposition of a piece of retinal tissue elicited a complete and reversible relaxation of a bovine retinal artery contracted with prostaglandin F2 alpha, suggesting that the inhibitory effect of adherent retinal tissue is mediated by a diffusible relaxing factor. Incubation of a bovine retina for 6 hours (37 degrees C, O2/CO2 95%/5%) yielded a solution which induced a relaxation of the retinal artery contracted with prostaglandin F2 alpha, further confirming the involvement of a diffusible chemical substance. The inhibitory effect of adherent retinal tissue on the contractile tone of isolated bovine retinal arteries could not be attributed to the release of NO, prostaglandins or adenosine. Nor did the characteristics of this factor correspond to any of the known vasoactive mediators formed within the retina. Further experiments demonstrated that the release of this elusive factor is probably linked to the oxygen tension, since hypoxia induced a vasodilation of preparations with adherent retinal tissue whereas preparations without retinal tissue were not affected by the change in oxygenation. The present work reveals a new form of intercellular communication in which (a) factor(s) derived from the retina profoundly relax(es) the smooth muscle cells of retinal arteries and hence modulate(s) retinal blood flow. The identity of this (these) factor(s) and the mechanisms by which this (these) factor(s) induce(s) vasodilation remain as yet to be determined.