Atrial natriuretic peptide , production

Atrial natriuretic peptide (ANP) is produced by specialized myocytes in the atria of the heart. Secretion is stimulated by increased filling and stretch of the atria in response to plasma volume expansion. The effects of ANP include vasodilation, diuresis (increased urine production), and increased sodium excretion. Taken together, these effects decrease blood volume and blood pressure toward normal. 

C. Clinical Role ANP has been studied for possible use in the treatment of congestive heart failure, but results have been mixed. BNP has showed some benefit in small studies in patients with heart failure. At present there are no clinically important products that act as agonists or antagonists at atrial natriuretic peptide receptors. 

The earliest endocrine abnormality in almost all types of cardiac disease is increased release of the heart s own hormones, the natriuretic peptides ANP and BNP (A for atrial, B for brain, where it was first discovered), and their concentration in plasma may become a guide to therapy. These peptides normally suppress renin and aldosterone production. 

Numerous neuroendocrine biomarkers correlate with severity of cardiac dysfunction. Heart failure is associated with increase in peripheral vascular resistance due to increases in sympathetic tone, norepinephrine, renin, angiotensin II, arginine vasopressin, and endothelin-1. The increased venous pressure causes atrial distension that stimulates production and release of atrial and brain natriuretic peptides (ANP, BNP) from the atria and ventricles, respectively. ANP inhibits the renin-angiotensin-aldosterone system. In humans and mammals, BNP has been found to be an early biomarker of left ventricular hypertrophy developing with doxorubicin cardiotoxicity, congestive heart failure, or occult dilated cardiomyopathy (Erkus et al. 2006 Walker 2006 Oyama, Sisson, and Solter 2007). 

---