Apparent mineralocorticoid excess syndrome Apparent mineralocorticoid excess syndrome Apparent mineralocorticoid excess (AME) is an autosomal recessive disorder causing hypertension (high blood pressure) and hypokalemia (abnormally low levels of potassium). It was found by Dr Maria I. New at Weil Cornell Hospital in New York City. It results from mutations in the "HSD11B2" gene, which encodes the kidney isozyme of 11β-hydroxysteroid dehydrogenase type 2. In an unaffected individual, this isozyme inactivates circulating cortisol to the less active metabolite cortisone. The inactivating mutation leads to elevated local concentrations of cortisol in the aldosterone sensitive tissues like the kidney. Cortisol at high concentrations can cross-react and activate
Subfornical organ excretion, blood volume regulation, and vasopressin secretion. The SFO is outside the blood–brain barrier, and so neuronal hormone receptors in this region can respond to factors present in the systemic circulation. The circumventricular organs express high density of Glucagon-like peptide 1 (GLP-1)receptors and participate in the central regulation of energy intake. Neurons in the subfornical organ have receptors for many hormones that circulate in the blood but which do not cross the blood–brain barrier, including angiotensin, atrial natriuretic peptide, endothelin and relaxin. The role of the SFO in angiotensin regulation is particularly important, as it is involved in communication with