MINERALOCORTICOID INDUCED HYPERTENSION

Several important advances have been made in the pathogenesis of miner alocorticoid induced hypertension. A hybrid gene was found to be respo nsible for glucorticoid remediable hypertension. This extra gene conta ins fragments of 11-beta0hydroxylase and aldosterone synthase. The hyb rid gene is the result of an unequal crossing-over of the two genes lo cated in close proximity on chromosome 8, and leads to the production of aldosterone and the hybrid steroils 18-hydroycortisol and 18-oxocor tisol. These hybrid steroids are also detected in patienta with aldost erone producing adenoma but not in patients with hyperald osterinism d ue to bilateral adrenal hyperplasia. In''Apparent Mineralocorticoid Ex cess'', inhertied as an autosomal recessive diorder, an increased rati o of urinary cortisol metabolite to cortisone is diagnostic. The syndr ome is due to a deficiency of the renal enzyme 11-beta-hydroxysteriod dehydrogenase type II, which protects the mineralocorticoid receptor a gainst cortisol that blinds to the mineralocorticoid receptor like ald osterone. Liddle's syndrome is a rare entity and due to a constitute a ctivation of an aldosterone dependent protein which triggers the amilo ride sensitive sodium channel in the kidney. This results in hypokalem ic hypertension with suppressed aldosterone and renin levels.