The mineralocorticoid receptor stabilizes epithelial sodium channels on the apical side of the cortical collecting duct principal cell, which increases sodium reabsorption, corresponding to peripheral edema, hypertension, and lower plasma renin activity (Figure 1), whereas potassium is excreted as a cationic ion via the renal outer medullary potassium channel, which results in hypokalemia and, in severe cases, myopathy or arrhythmia (1). Here, NR3C2 is linked to Hypertension.