Hypertension is a common condition, which, depending on its definition, affects 10-25% of the population. Because it is an established risk factor for coronary and cerebrovascular disease, hypertension has, quite rightly, been targeted as an important factor in determining the health of the nation. Despite this we can explain the underlying cause of a patient's hypertension in Ͻ5% of cases; the remainder are labelled 'essential' hypertension, an elegant way of stating that the aetiology is unknown. As a result, in the vast majority of cases treatment is given on an empirical basis.In the last 5 years, significant advances have been made in our understanding of the pathogenesis of hypertension with the characterisation of three forms of inherited hypertension. All arise because of distinct, single gene mutations but can result in the same phenotype, that of mineralocorticoid hypertension. The purpose of this article is to review these 'monogenic' forms of mineralocorticoid hypertension, glucocorticoid-remediable hyperaldosteronism, Liddle's syndrome and apparent mineralocorticoid excess, and to discuss their significance to the broader population with essential hypertension.Glucocorticoid remediable aldosteronism (GRA) (also referred to as dexamethasone suppressible hyperaldosteronism or glucocorticoidsuppressible hyperaldosteronism)In 1966 a hypertensive father and son were described with a new disorder that mimicked priCorrespondence: PM Stewart, Professor