There is clear evidence for rapid nongenomic effects of aldosterone in the cardiovascular system in addition to its well characterized effects of unidirectional transepithelial sodium transport. Many of these effects are mediated by the classical mineralocorticoid receptors, although others may be exerted independently. Given that mineralocorticoid receptors are largely constitutively occupied but not activated by physiological glucocorticoids, effects of aldosterone administered in vitro or in vivo may or may not equate with true physiological mineralocorticoid roles. In many systems (e.g. blood pressure regulation and cardiac fibrosis), the time course of effects is such that it is not possible, and perhaps not important, to distinguish between rapid nongenomic and classical genomic effects in the context of homeostatic physiology.