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The atrial natriuretic factor is a 28-amino-acid peptide with a 17-amino-acid ring in the middle. A disulfide link connects two cysteine residues at positions 7 and 23 to produce the ring. Atrial natriuretic factor shares an amino acid ring structure with BNF (brain natriuretic factor) and CNF (C-type natriuretic factor). It is one of the nine structurally related natriuretic hormones, seven of which are produced by the heart.

Types of atrial natriuretic factor receptors

There are three types of atrial natriuretic peptide receptors on which natriuretic factors operate. They are all cell surface receptors with different names. They are:

  • Natriuretic peptide receptor-A or NPR1
  • Natriuretic peptide receptor-B or NPR2
  • Natriuretic peptide clearance receptor or NPR3

 Role of Atrial Natriuretic Factor

  • It operates on the kidney to promote salt excretion and Glomerular Filtration Rate (GFR), limit renin secretion, and counteract renal vasoconstriction.
  • It inhibits vasoconstriction in the cardiovascular system and moves fluid from the intravascular to the interstitial compartment.
  • It influences the natriuretic response to acute and chronic volume overload. The ability of ANF to move fluid out of the circulatory system is one of its most notable features.
  • It is a potent inhibitor of aldosterone synthesis in the adrenal gland.
  • It moves fluid from the vascular to the interstitial compartment and functions as a buffer, preventing excessive plasma volume expansion in response to an increase in total extracellular fluid volume.
  • When salt excretion is threatened by a reduction in the number of nephrons, ANF acts as a physiological regulator of Glomerular Filtration Rate (GFR), mediating nephron hyperfiltration and natriuresis.  

Cause of ANF secretion

The 28-amino-acid polypeptide hormone ANF is released primarily by the heart atria in response to atrial stretch. ANF is produced in response to the following stimuli:

  • Stretching of the atrial wall by atrial volume receptors
  • Increase in sympathetic activation of adrenoceptors
  • Increased sodium concentration (hypernatremia). However, it is not the direct cause of increased ANP secretion.
  • Presence of a powerful vasoconstrictor, endothelin

Physiological effects of Atrial Natriuretic Factor (ANF)

1.Renal

ANF stimulates sodium and water excretion in the kidneys. It happens in the following way:

  • The main location of ANP control of sodium excretion is the medullary collecting duct.
  • The glomerular filtration rate and permeability are both increased by ANF. ANF dilates the afferent arteriole directly, counteracting the afferent arteriole’s vasoconstriction caused by norepinephrine.
  • Increases blood flow through the vasa recta, allowing the solutes (NaCl and urea) to be washed out of the medullary interstitium.
  • It reduces sodium reabsorption in the nephron’s thick ascending limb and cortical collecting duct.
  • It prevents the formation of angiotensin and aldosterone by suppressing renin secretion.
  • It suppresses the sympathetic nervous system of the kidneys.

2.Adrenal

It reduces aldosterone secretion by the adrenal cortex’s zona glomerulosa.

3.Vascular

It relaxes the smooth muscle of the circulatory system in arterioles and venules by:

  • Increasing vascular smooth muscle mediated by membrane receptors
  • Inhibiting actions of catecholamines 
  • Encouraging uterine spiral artery remodelling, which is critical for reducing pregnancy-induced hypertension.

4.Cardiac

  • ANF prevents myocardial hypertrophy and fibrosis in heart failure. Fibrosis is slowed by preventing fibroblasts from entering and multiplying in the heart tissue and reducing inflammation.
  • ANF inhibits hypertrophy by decreasing norepinephrine-induced calcium influx.
  • The phenotype is saved when NPRA is re-expressed.

5.Immune system

Several immune cells manufacture ANF locally. ANF has been demonstrated to have cytoprotective effects and regulate various aspects of the innate and adaptive immune systems.

  • ANF affects innate immunity by increasing defence against extracellular microorganisms while also suppressing the production of pro-inflammatory signals and adhesion molecule expression.
  • In myocardial, vascular smooth, endothelial, hepatocytes, and tumour cells, ANP has been shown to have cytoprotective properties.

6.Adipose tissue

  • Increases release of free fatty acids from adipose tissue. In humans, I.V. Infusion of ANF increases plasma concentrations of glycerol and unsaturated fatty acids.
  • Increases intracellular cGMP levels, which causes a hormone-sensitive lipase and perilipin to be phosphorylated. 

Conclusion

The excitement around the discovery of ANF stemmed in part from the fact that its physiological job appeared to be straightforward. Because of ANF’s strong natriuretic properties and its position in the cardiac atria, it may be responsible for the increase in salt and water excretion that occurs when atrial chamber pressure rises. 

ANF production has been detected in tissues other than the cardiac atria, and receptor binding studies have revealed organs other than the kidneys as target organs. As a result, it is safe to assume that our understanding of ANF’s physiological role will need to evolve in the coming years.