Atrial myocytes synthesise atrial natriuretic factor prohormone consisting of 126 amino acids (ANP1-126) which is subsequently processed to several fragments. Atrial natriuretic factor (ANF, ANP99-126) originating from the C-terminal portion of prohormone is a best described atrial peptide. However, several peptides originating from the N-terminus of this precursor also circulate and produce significant diuresis, natriuresis and vasodilatation. These are: long acting natriuretic peptide (ANP1-30), vessel dilator (ANP31-67) and kaliuretic peptide (ANP79-98). ANP1-98 and ANP68-98 also circulate. Kaliuretic peptide specifically stimulates urinary potassium excretion. These peptides are slowly metabolised and their plasma concentration is higher than ANF suggesting their important role in water-electrolyte homeostasis and regulation of vascular tone. N-terminal atrial peptides don't bind to classical natriuretic peptide receptors, each of them has probably its own unique receptors. Although these peptides activate particulate guanylate cyclase in a number of tissues, some of their effects, for example natriuresis, are not mediated by cGMP but rather by prostaglandin E2. Plasma concentration of N-terminal atrial peptides may be useful in diagnosis and risk stratification in patients with heart failure and after myocardial infarction. Recently N-terminal fragment of brain natriuretic peptide (BNP1-76) was identified in the blood. This peptide is secreted together with its C-terminal partner, BNP77-108 by ventricular myocytes. Some studies suggest that N-terminal BNP may be also a useful diagnostic tool in cardiovascular diseases.