Aldosterone
| Net effect | Na retention, K loss |
|---|---|
| Secreted from | ZG of Adrenal cortex |
| Stimulus | - ↑ Angiotensin II - ↑ K - ↑ ACTH - fluid loss (as per atrial stretch receptors)/ hypotension |
| Inhibition | |
| Site of action | Distal tubules, collecting ducts |
| Action (function) | - Up regulation of basolateral Na+-K+ pumps - Up-regulation of epithelial sodium channels (ENaCs) in the collecting duct |
intracellular effects of aldosterone
at principal cells of distal convoluted tubule
- Increases expression of ROMK channels
- Increases expression of ENaC channels on apical membrane
at alpha intercalated cells of collecting duct
- Increases activity of the Na+-K+-ATPase on the basolateral membrane
- increases expression of H+/ATPase on apical membrane
→ results in ↑ H+ in lumen (i.e. excretion)
Primary hyperaldosteronism
| AKA Conn's syndrome | |
|---|---|
| Etiology | either adrenal adenoma or idiopathic adrenal hyperplasia |
| Clinical presentation | Hypertension Hypokalaemia, hypernatraemia, volume overload Metabolic alkalosis (from ↑ H+ secretion into tubules) The hypokalaemia may cause muscle paralysis |
| Diagnostic investigations | ↑ aldosterone, ↓ renin |
| Management | - Surgical resection of adenoma - Aldosterone antagonist - e.g. spironolactone |