Does aldosterone increase or decrease sodium levels?

From the Guidelines

Aldosterone increases sodium levels in the body by stimulating renal sodium reabsorption. This effect is primarily mediated through the action of aldosterone on the distal tubules and collecting ducts of the kidneys, where it increases the permeability of the luminal membrane of principal cells to sodium and the activity of the Na/K ATPase pump in the basolateral membrane 1. The increased reabsorption of sodium along the distal tubule is mostly related to hyperaldosteronism, as noted in patients with cirrhosis and ascites 1. Key points to consider include:

• Aldosterone antagonists are more effective than loop diuretics in the management of ascites and are the diuretics of choice 1
• The dosage of antialdosteronic drugs should be increased every 7 days due to the slow effect of aldosterone, which involves interaction with a cytosolic receptor and then a nuclear receptor 1
• The use of aldosterone antagonists, such as spironolactone, is recommended as the initial treatment for patients with a first episode of ascites, with the option to add a loop diuretic like furosemide if necessary 1.

From the FDA Drug Label

Spironolactone and its active metabolites are specific pharmacologic antagonists of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Increased levels of the mineralocorticoid, aldosterone, are present in primary and secondary hyperaldosteronism. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained

Aldosterone increases sodium reabsorption in the kidneys. Since spironolactone is an aldosterone antagonist, it counteracts the effects of aldosterone, leading to increased sodium excretion. Therefore, aldosterone itself increases sodium reabsorption, which means it decreases sodium excretion. 2

From the Research

Aldosterone's Effect on Sodium

• Aldosterone stimulates the reabsorption of sodium in the kidneys, which helps to sustain blood volume and pressure 3.
• The hormone regulates sodium homeostasis, thereby helping to control blood volume and blood pressure 4.
• Elevated serum aldosterone levels increase blood pressure largely by increasing Na+ re-absorption in the kidney through regulating transcription and activity of the epithelial sodium channel (ENaC) 5.
• Aldosterone's action on sodium reabsorption is a key factor in its role in regulating blood pressure and fluid balance in the body.

Mechanisms of Aldosterone's Action

• Aldosterone synthesis is primarily regulated by angiotensin II, K+ concentration, and adrenocorticotrophic hormone 5, 4.
• The signaling pathways involved in aldosterone synthesis and its effects on Na+ reabsorption include phospholipase C-mediated phosphoinositide hydrolysis, inositol 1,4,5-trisphosphate, cytosolic calcium levels, and calcium/calmodulin-dependent protein kinases 4.
• Aldosterone's effects on the kidney and other tissues are mediated by its binding to mineralocorticoid receptors, which triggers a cascade of signaling events that ultimately lead to increased sodium reabsorption and water retention 3, 5.

Clinical Implications

• Excessive aldosterone levels can cause hypertension and exacerbate the effects of high blood pressure on multiple organs, contributing to renal disease, stroke, visual loss, and congestive heart failure 6, 4.
• Aldosterone receptor antagonists, such as spironolactone and eplerenone, have been shown to be effective in reducing morbidity and mortality in patients with heart failure and hypertension 6, 7.
• The use of aldosterone receptor antagonists may be associated with an increased risk of hyperkalemia, particularly in patients with renal impairment or those taking other medications that affect potassium levels 7.