The actions of aldosterone on Vmax Na+-K+-ATPase activity and length of latent period were assessed for the rabbit cortical collecting duct (CCD). Initially, animals were moderately aldosterone depleted and then treated with a constant infusion of physiological doses of aldosterone. Aldosterone administration had no influence after 3 h but caused a detectable increase with 6 (borderline significance) or more hours. An apparent plateau was reached between 24 and 48 h at twice the initial activity. This aldosterone-induced stimulation could be abolished by simultaneous treatment of the animals with amiloride, demonstrating a Na+-dependent modulation of the Vmax Na+-K+-ATPase activity. The aldosterone-stimulated enzyme had kinetic properties similar to those reported by others, but the latent period for aldosterone action on the Vmax Na+-K+-ATPase activity averaged near 6 h in the present study, as opposed to the highly variable period (from 1 h to several days) seen by others. This latent period variability was shown to be directly related to the initial Vmax Na+-K+-ATPase activity in the CCD and could be likened to an "end product dependent" latent period, i.e., the lower the initial end product (Vmax Na+-K+-ATPase activity) the shorter the latent period. Hence aldosterone's actions on the Na+-K+-ATPase of the CCD would be consistent with a single mechanism of action, i.e., increased synthesis, but with a variable modulation of this synthesis, which is dependent on the initial Vmax Na+-K+-ATPase activity of the CCD cells and/or the initial aldosterone status of the animal.