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Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.
Aldosterone is the primary of several endogenous members of the class of mineralocorticoids in humans. [citation needed] Deoxycorticosterone is another important member of this class. Aldosterone tends to promote Na + and water retention, and lower plasma K + concentration by the following mechanisms:
In summary, hyperaldosteronism causes hypernatremia, hypokalemia, and metabolic alkalosis. [13] Finer notes on aldosterone include the fact that it stimulates sodium-potassium ATPase in muscle cells, increasing intracellular potassium and also increases sodium reabsorption all along the intestine and nephron, possibly due to widespread ...
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 physiology, aldosterone escape is a term that has been used to refer to two distinct phenomena involving aldosterone that are exactly opposite each other: Escape from the sodium -retaining effects of excess aldosterone (or other mineralocorticoids ) in primary hyperaldosteronism , manifested by volume and/or pressure natriuresis .
The primary endogenous mineralocorticoid is aldosterone, although a number of other endogenous hormones (including progesterone [1] and deoxycorticosterone) have mineralocorticoid function. Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption of water, as well as the active secretion of ...
Thus, dysfunction of the pituitary gland or the hypothalamus does not affect the production of aldosterone. [2] [3] However, in primary adrenal insufficiency, damage to the adrenal cortex (e.g. autoimmune adrenalitis a.k.a. Addison's disease) can lead to destruction of the zona glomerulosa and therefore a loss of aldosterone production.
dRTA commonly leads to sodium loss and volume contraction, which causes a compensatory increase in blood levels of aldosterone. [4] Aldosterone causes increased resorption of sodium and loss of potassium in the collecting duct of the kidney, so these increased aldosterone levels cause the hypokalemia which is a common symptom of dRTA.