High blood pressure under these conditions is thought to be partially mediated by inappropriate activation of the mineralocorticoid receptor (MR) by the higher circulating concentrations of glucocorticoid in the distal tubule, since corticosterone and aldosterone have equal affinity for MR, ultimately resulting in greater salt-retention - in extremis this is known as the syndrome of Apparent Mineralocorticoid Excess [26]. The gene discussed is NR3C2; the disease is hypertensive disorder.