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This is not Dr Conn s aldosterone anymore Brown NJTrans Am Clin Climatol Assoc 2011[]; 122 (ä): 229-43In 1955, Dr. Jerome Conn described a patient with severe hypertension and hypokalemia and an aldosterone-secreting adenoma. The prevalence of hyperaldosteronism is increased among patients with obesity or resistant hypertension. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers reduce the secretion of aldosterone, but with chronic treatment aldosterone concentrations "escape" back to baseline values. Mineralocorticoid receptor (MR) antagonism reduces mortality in patients with heart disease who are already taking an ACE inhibitor and diuretic. In addition to affecting sodium and potassium homeostasis via classical MR-dependent pathways, aldosterone induces inflammation and causes cardiovascular remodeling and renal injury. Some of these effects involve MR-independent pathways. At the same time, ligands other than aldosterone can activate the MR. This paper reviews mechanism(s) for the proinflammatory and profibrotic effects of aldosterone and presents data indicating that endogenous aldosterone, acting at the MR, contributes to many of the pro-inflammatory and pro-fibrotic effects of angiotensin II in vivo.|*Signal Transduction/drug effects[MESH]|Aldosterone/administration & dosage/blood/*metabolism[MESH]|Angiotensin II Type 1 Receptor Blockers/pharmacology[MESH]|Angiotensin II/metabolism[MESH]|Angiotensin-Converting Enzyme Inhibitors/pharmacology[MESH]|Animals[MESH]|Blood Pressure/drug effects[MESH]|Cytochrome P-450 CYP11B2/antagonists & inhibitors/metabolism[MESH]|Disease Models, Animal[MESH]|Enzyme Inhibitors/pharmacology[MESH]|Fibrosis[MESH]|Gene Expression Regulation[MESH]|Humans[MESH]|Hyperaldosteronism/drug therapy/genetics/*metabolism/pathology/physiopathology[MESH]|Inflammation Mediators/metabolism[MESH]|Kidney/drug effects/*metabolism/pathology[MESH]|Ligands[MESH]|Mice[MESH]|Mineralocorticoid Receptor Antagonists/pharmacology[MESH]|Myocardium/*metabolism/pathology[MESH]|Rats[MESH]|Receptors, Mineralocorticoid/metabolism[MESH]|Time Factors[MESH] |
