Polypeptide secreted by atrial cells when the atrium is distended.
Secreted in response to signals from myocardial stretch and volume overload.
Produced with its inactive amino terminal fragment NT-proANP.
Can produce vasodilation, natriuresis and diuresis during hypertension and congestive heart failure.
Inhibits renin and aldosterone secretion, sympathetic nervous system, cardiac fibrosis and hypertrophy, and improves diastolic function and introduces metabolic protective properties along with BNP.
Atrial distention due to volume expansion with saline, water immersion, postural changes, and salt intake resulting in an increased plasma atrial natriuretic peptide.
Has no predictive value for cardiovascular mortality or morbidity.
Increased circulating volume is the most important stimulant of ANP release.
Other factors increasing ANP release include endothelin, platelet activating factor, corticotropin-releasing factor, and glucagon like peptide-1 can trigger the synthesis of ANP.
ANP is synthesized as a 151 amino acid pre-pro hormone and is stored in atrial myocytes as a 126 amino acid pro hormone (pro-ANP).
When secreted, pro-AN P is cleaved yielding N-ANP and active C-terminal hormone ANP.