What would be the physiological consequences of overproduction of aldosterone by the zona glomerulosa of the adrenal glands?
Aldosterone is the major mineralocorticoid in human.
It is regulated by three important stimulus- angiotensin II , ACTH and plasma potassium concentration.
Aldosterone - mechanism of action
Aldosterone binds with cytoplasmic receptor. The HR complex moves to the nucleus where it induces this is transcription of mRNA.
This increases new protein synthesis that alters the cell function. Aldosterone has genomic actions and non genomic actions-
Genomic actions - The gene activated by aldosterone is sgk gene(serum and glucocorticoid regulated gene). Aldosterone increases ENaC (epithelial sodium channels) activity.
Nongenomic action- There is simulation of activity of sodium-potassium exchanger which increases the intracellular accumulation of sodium.
Aldosterone dysfunction--
Primary hyperaldosteronism - the cause of excess aldosterone secretion is due to the adrenal disease the usual cause are aldosterone producing adrenal adenoma (Conn's syndrome) , adrenal hyperplasia and adrenal carcinoma.
Rennin secretion is decreased in primary hyperaldosteronism.
Conn's syndrome-
This is the major cause of primary hyperaldosteronism. It occurs due to the tumor of the zona glomerulosa of adrenal cortex.
The disease manifest with hypertension (due to sodium retention and ECF expansion), muscle weakness and fatigue (due to potassium depletion and polyuria (due to impairment of urinary concentrating ability).Edema is not usually a feature of primary hyperaldosteronism.
Hypokalemia, hyponatremia and low renin plasma and metabolic alkalosis are the findings
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