Atrial natriuretic peptide (ANP) or Atrial natriuretic factor (ANF) is a peptide hormone which reduces an expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized, and secreted by cardiac muscle cells in the walls of the atria in the heart. These cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume. ANP is one of a family of nine natriuretic peptides: seven are atrial in origin.
ANP acts on the kidney to increase sodium and water excretion (natriuresis) in the following ways: 1) it dilates the glomerular afferent and constricts efferent arterioles, and relaxes the mesangial cells. This increases pressure in the glomerular capillaries, increasing the glomerular filtration rate (GFR), resulting in an increased amount of sodium and water being filtered and excreted. 2) It increases blood flow through the vasa recta, which washes the solutes sodium chloride (NaCl) and urea out of the medullary interstitium – the lower osmolarity here leads to less reabsorption of tubular fluid and increased excretion. 3) It decreases sodium reabsorption in the distal convoluted tubule and cortical collecting duct. 4) It inhibits renin secretion, thereby inhibiting the production of angiotensin and aldosterone. 5) It inhibits the renal sympathetic nervous system. ANP has the opposite effect of aldosterone on the kidney: aldosterone increases renal sodium retention and ANP increases renal sodium loss.[5][6]
Reduction of blood volume by ANP can result in secondary effects such as reduction of extracellular fluid (ECF) volume (edema), improved cardiac ejection fraction with resultant improved organ perfusion, decreased blood pressure, and increased serum potassium. These effects may be blunted or negated by various counter-regulatory mechanisms operating concurrently on each of these secondary effects.
