Aldosterone stimulates sodium reabsorption across tight epithelia via corticosteroid receptors. These receptors are ligand-activated transcription factors which regulate a set of genes, leading to changes in the expression of proteins which are thought to mediate the stimulatory action on sodium reabsorption. This functional response starts after a lag period and can be schematically divided into an early phase of activation and a late phase of accumulation of effectors such as Na<sup>+</sup> channels and pumps. Recently, the first gene products regulated sufficiently rapidly by aldosterone to possibly account for the early activation have been identified. However, the actual mediators of the physiological response remain to be determined. Besides these transcriptionally mediated effects, aldosterone has been shown to produce rapid, nongenomic actions on intracellular signalling cascades leading to an activation of Na<sup>+</sup>/H<sup>+</sup> exchange. Such effects are mediated by a different type of receptor and have been described both in classical aldosterone target cells and other cells. Their physiological implications are as yet not clear. The aim of this minireview is to describe briefly both the classical early and rapid nongenomic effects of aldosterone and to address the question whether nongenomic effects might play a role for the Na<sup>+</sup> transport response.