Atrial natriuretic peptide

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natriuretic peptide precursor A
Identifiers
Symbol	NPPA ANP, PND
HUGO	7939
Entrez	4878
OMIM	108780
RefSeq	NM_006172
UniProt	P01160
Other data
Locus	Chr. 1 p36.21

Atrial natriuretic factor (ANF), atrial natriuretic peptide (ANP) or atriopeptin, is a polypeptide hormone involved in the homeostatic control of body water, sodium, and adiposity. It is released by atrial myocytes, cells in the atria of the heart, in response to signals of raised blood pressure and acts to reduce the water, sodium and adipose loads on the circulatory system, thereby returning blood pressure to more normal levels.

Contents 1 Structure 2 Production 3 Receptors 4 Physiological effects 4.1 Renal 4.2 Vascular 4.3 Adipose tissue 5 Degradation 6 Other natriuretic factors 7 Medical Laboratory Diagnostic Use 8 See also 9 References 10 External links

[edit] Structure

ANP is a 28 amino acid peptide with a 17 AA ring, and is closely related to BNP (brain natriuretic peptide) and CNP (C-type natriuretic peptide) which all share the same amino acid ring. ANP was discovered in 1981 by a team in Ottawa led by Adolfo J. de Bold after they made the seminal observation that injection of atrial (but not ventricular) tissue extracts into rats caused copious natriuresis.^[1]

[edit] Production

ANP is produced, stored and released by cells present in the atria of the heart, atrial myocytes. It is released in response to a variety of signals, the signals, present when the subject is hypervolaemic, exercised or calorically restricted.

It is secreted in response to:

• Atrial distention, stretching
• Sympathetic stimulation of β-adrenoceptors
• Raised sodium concentration
• Angiotensin-II
• Endothelin, a potent vasoconstrictor

Causes of stretching include high extracellular fluid volume, high blood volume, and atrial fibrillation. Notably, it is secreted in response to immersion of the body in water, which causes an atrial stretch due to altered distribution of intravascular fluid. It has been shown that in horses, it is also released in response to exercise.

[edit] Receptors

See atrial natriuretic factor receptors

[edit] Physiological effects

The overall effects of ANP release are a reduction in blood volume and therefore a reduction in central venous pressure, cardiac output, and arterial blood pressure. It increases renal sodium secretion and excretion. It also increases lipolysis.

The overall effect of which is to counter the blood pressure-raising effects of the renin-angiotensin system.

[edit] Renal

• Dilates the afferent glomerular arteriole, constricts the efferent glomerular arteriole, and relaxes the mesangial cells. This increases the glomerular filtration rate, resulting in greater excretion of sodium and water.

• Decreases sodium resorption in the renal distal convoluted tubule and cortical collecting duct.As an effect of inhibiting of the renin-angiotensin system.

• Inhibits renin secretion.

• Reduces aldosterone secretion by the adrenal cortex.

[edit] Vascular

• Relaxes vascular smooth muscle in arterioles and venules by:
  • Receptor-mediated elevation of vascular smooth muscle cGMP
  • Inhibition of the effects of catecholamines

[edit] Adipose tissue

• Increases the release of free fatty acids from adipose tissue. Plasma concentrations of glycerol and nonesterified fatty acids are increased by i.v. infusion of ANP in humans.
• Activates adipocyte plasma membrane type A guanylyl cyclase receptors NPR-A
• Increases intracellular guanosine 3',5'-cyclic monophosphate cyclic GMP levels that induce the phosphorylation of a hormone-sensitive lipase and perilipin A via the activation of a cGMP dependent protein kinase-I cGK-I
• Does not modulate cAMP production or PKA activity

[edit] Degradation

Degradation of ANP is needed for its actions to be stopped. It is broken down by an enzyme, neutral endopeptidase (NEP). Recently inhibitors of NEP have been developed, although have not yet been licensed, proving to be beneficial in congestive heart disease.

[edit] Other natriuretic factors

In addition to the mammalian natriuretic factors (ANP, BNP, CNP), two other peptides have been isolated. Tervonen (1998) described a salmon natriuretic factor (Salmon cardiac peptide) with a similar structure and properties^[2] and Dendroaspis Natriuretic Peptide (DNP) was discovered in the venom of the green mamba by Schweitz et al. (1992).

[edit] Medical Laboratory Diagnostic Use

Used in conjunction with other clinical information, measurement of B-type natriuretic peptide (BNP) can be made to differentiate between causes of dyspnea due to congestive heart failure (CHF)-- where BNP levels are elevated-- from that of other causes of dyspnea.

This laboratory test has become a valuable and quick method for diagnostic work-up of patients presenting to the emergency department (ED) with acute dyspnea.

[edit] See also

• Atrial volume receptors

[edit] References

1. ^ de Bold A (1985). "Atrial natriuretic factor: a hormone produced by the heart.". Science 230 (4727): 767-70. PMID 2932797. 
2. ^ Tervonen et al., 1998 Endocrinology 139:4021-4025.

[edit] External links

• MeSH Atrial+Natriuretic+Factor