The nature and the mechanisms of renal Na,K-ATPase (Na pump) regulation by corticosteroids remain a matter of debate. This is mainly due to the limitations of the experimental approaches, the inhomogeneity of the nephron and the complexity of homeostatic feedback mechanisms. However, 'classical' early and late cellular actions of corticosteroids, which are mineralocorticoid-specific in the collecting duct, can be recognized: The 'early action' is characterized by an increase in the number of active (versus inactive) pumps and/or by a change in their kinetic properties. The 'late action' is characterized by an increase in the number of pumps resulting from, at least in part, an increase in the rate of Na,K-ATPase gene transcription. Sodium delivery into the cells and other elements of the regulatory network play permissive or co-regulatory roles in both early and late actions.