Pulsatile injections of cyclic GMP into rod outer segments of the isolated toad retina cause transient depolarizations that are reduced in amplitude in proportion with the receptor potential by low Na+ Ringer's. This reduction in the amplitude of the cyclic GMP depolarization may be due to the direct effect of external Na+ concentration on dark current and an indirect effect resulting from the inactivation of a sodium-calcium exchange mechanism raising the intracellular Ca2+ concentration. By comparison the reduction in cyclic GMP response amplitude effected by illumination is accompanied by faster kinetics. This difference suggests that the reduced amplitude and speedier response reflect a light induced increase in phosphodiesterase (PDE) activity rather than the effects of Ca2+. Large doses of cyclic GMP can distort the kinetics of both the light response and the recovery from a depolarization caused by a pulse of cyclic GMP by similarly slowing both types of responses. This similarity in the kinetics of the cyclic GMP response and the initial hyperpolarizing phase of the receptor potential suggests that the kinetics of the initial phase of the receptor potential are controlled by light-mediated cyclic GMP hydrolysis.