Specific Binding of Nicergoline on an α1-like Adrenoreceptor in the Rat Retina

Systemic treatment with nicergoline, an ergoline derivative showing α1‐antagonist properties, causes vasodilatation in the eye without apparent untoward cardiovascular effects. In the present work we investigated the ability of nicergoline to inhibit the binding of radiolabeled prazosin in the rat retina and cortex. We found that nicergoline inhibited [3H]prazosin binding in both tissues, being more potent than unlabelled prazosin in the retinal tissue. The competition curves of the ergoline derivative were well fitted by a one‐site model in the cortical tissue, with an IC50 (concentration of the drugs needed to inhibit the binding of labelled prazosin by 50%) of 2.54 times 10−8 M, and by a two‐site model in the retinal tissue, with IC50 values of 7.08 times 10−12 M and 1.82 times 10−5 M. 2‐(2,6 dimetoxyphenoxyethyl) aminomethyl‐1,4‐benzodioxane hydrochloride (WB4101) and phentolamine, selective ligands for the high‐affinity binding site for prazosin, in particular the α1A‐site, fully inhibited prazosin binding in the cortex but only partially inhibited prazosin binding in the retina, being less potent in this tissue than either nicergoline or prazosin. Our results suggest that a binding component of α1‐adrenoceptors is expressed to a lesser extent in the retina than the cortex, leading to a reduced response of the retinal tissue to prazosin, and more particularly to WB4101 and phentolamine. The selective binding of the nicergoline on this retinal adrenoreceptor may explain the peculiar efficacy of the drug in ocular pathophysiology.