natriuresi

Natriuresis is the process by which the kidneys excrete sodium in the urine, balancing sodium intake with loss to regulate extracellular fluid volume and blood pressure. Sodium is freely filtered at the glomerulus, but most is reabsorbed along the nephron. Natriuresis refers to the net amount of sodium that is not reabsorbed and is eliminated in urine.

Key regulators include aldosterone, which stimulates sodium reabsorption in the distal tubule and collecting duct, thereby decreasing natriuresis. Natriuretic peptides, such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), promote natriuresis by increasing glomerular filtration and reducing sodium reabsorption in the collecting ducts. Other influences include dopamine and the renal effects of the sympathetic nervous system. Pressure natriuresis describes how increases in effective arterial blood volume and blood pressure can raise sodium excretion independent of hormonal changes.

Clinically, natriuresis is assessed by measuring urine sodium concentration or the fractional excretion of sodium (FENa). It is a component of the body’s response to diuretic therapy and plays a role in conditions that alter volume status, such as heart failure or kidney disorders. Natriuresis can accompany diuresis, but the terms describe different endpoints: solute excretion versus urine volume.

In summary, natriuresis reflects the kidney’s regulation of sodium balance and extracellular fluid volume. It is influenced by hormonal and hemodynamic factors and can be modulated by medications that alter tubular sodium handling. Understanding natriuresis helps explain how the body maintains blood pressure and electrolyte homeostasis.