The light-induced constriction of the irises of some vertebrates is mediated by photosensitive pupillary sphincter cells, which have rhodopsin molecules in their sarcolemmas. Light-induced isomerization of these rhodopsin molecules leads to the release of Ca2+ from an internal pool, which in turn activate the contractile proteins. A central nervous reflex is therefore not essential for the light responsiveness of these irises, but they do appear to be innervated. The photosensitive iris of the toad receives sympathetic (adrenergic) innervation. Stimulation of sympathetic nerves to the eye or application of adrenergic agonists to the iris cause pupillary dilation due to relaxation of the sphincter muscle. We show here that beta-adrenergic stimulation of toad sphincter cells modulates their photoresponses by elevating the intracellular levels of cyclic AMP. However, cyclic AMP does not appear to be involved in the transduction event but rather alters the availability of Ca2+ for contraction.