In 1955, Conn described a special form of hypertension caused by a tumor in humans aldestoronprodutsiruyuschey glomerular zone of adrenal cortex.
Clinical and laboratory manifestations of the syndrome are due to Conn's excess aldosterone in the body - the main mineralocorticoid hormone, which stimulates the reabsorption of sodium (mainly in the distal tubule kidney). Stimulators of aldosterone synthesis and release are the norm reducing the concentration of sodium and increase potassium levels in the serum decrease in blood volume ACTH angiotensin II.
Sodium retention due to hyperaldosteronism, hypernatraemia causes, as a result of this increased output of antidiuretic hormone, which causes water retention and increased blood volume. Increased blood volume leads to an increase in cardiac output and peripheral resistance. Sodium and water retention leading to swelling of the walls of the arterioles, narrowing of their lumen, increased peripheral resistance. These two mechanisms responsible for hypertension.
Strengthening the sodium retention in the kidneys leads to increased excretion of potassium and hypokalemia. Hypokalemia clinically manifested muscle weakness. Often, these patients with a diagnosis of "myasthenia" for many years carried out in a neurological hospital. Sometimes there jerking of the muscles and parastezii, numbness, and violations of the type of flaccid paralysis. These symptoms are worse in winter and spring, when a little potassium diet.
Prolonged hypokalemia causes a characteristic degenerative changes in the heart muscle, nephropathy, which manifests polyuria, dehydration, thirst. For primary aldosteronism is characterized by increasing the ratio of Na \ K, which is normally 30-32. In identifying the surgical treatment aldosteronoma, the prognosis is mainly good.