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It selectively stimulates secretion of aldosterone. The secretion of aldosterone has a diurnal rhythm. Control of aldosterone release from the adrenal cortex: [citation needed] The role of the renin–angiotensin system: Angiotensin is involved in regulating aldosterone and is the core regulator. Angiotensin II acts synergistically with potassium.
In cases due to enlargement of both glands, treatment is typically with medications known as aldosterone antagonists such as spironolactone or eplerenone. [1] Other medications for high blood pressure and a low salt diet, e.g. DASH diet, may also be needed. [1] [4] Some people with familial hyperaldosteronism may be treated with the steroid ...
Treatment includes removing the causative agent (such as licorice), a high-potassium, low-sodium diet (for primary) and high-sodium diet (for secondary), spironolactone and eplerenone, potassium-sparing diuretics that act as aldosterone antagonists, and surgery, depending on the cause. [11] For adrenal adenoma, sometimes surgery is performed.
Drugs that interfere with the secretion or action of aldosterone are in use as antihypertensives, like lisinopril, which lowers blood pressure by blocking the angiotensin-converting enzyme (ACE), leading to lower aldosterone secretion. The net effect of these drugs is to reduce sodium and water retention but increase the retention of potassium.
Specific treatment of pseudohyperaldosteronism depends on the inciting cause. General management focuses on countering the effects of excess mineralocorticoid activity to achieve adequate blood pressure control and avoid end-organ damage and cardiovascular mortality. [1] In some cases, specific antihypertensive medications may be recommended.
Familial hyperaldosteronism is a group of inherited conditions in which the adrenal glands, which are small glands located on top of each kidney, produce too much of the hormone aldosterone. [1] Excess aldosterone causes the kidneys to retain more salt than normal, which in turn increases the body's fluid levels and causes high blood pressure. [1]
In the adrenal cortex, angiotensin II acts to cause the release of aldosterone. Aldosterone acts on the tubules (e.g., the distal convoluted tubules and the cortical collecting ducts) in the kidneys, causing them to reabsorb more sodium and water from the urine. This increases blood volume and, therefore, increases blood pressure.
On one hand, mutations on the gene NR3C2 (coding the mineralocorticoid receptor) cause the synthesis of a non-functional receptor which is unable to bind aldosterone or function correctly. In the kidney, aldosterone plays an important role of regulating sodium and potassium homeostasis by its actions on distal nephron cells. [3]