Cortisol and aldosterone bind the MR with equal affinity, but cortisol levels are significantly higher relative to aldosterone and, thus, occupy these receptors. The enzyme 11β-HSD2 acts to convert cortisol to cortisone, which is unable to bind the MR, thus allowing aldosterone to bind the available receptors. Once bound, the MR can translocate to the nucleus and engage DNA promoter sites to affect transcription and translation (genomic effects). Aldosterone can also mediate rapid nongenomic effects via the MR, which does not involve gene expression and protein synthesis.