Heart natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) act as key regulators of homeostasis of body fluids volume and blood pressure, by decreasing salt excess and water retention, and by inhibiting intensive action of sympathetic nervous system and secretion of vasoconstrictor hormones. Plasma ANP, N-terminal pro-atrial natriuretic peptide (NT-proANP), BNP and N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations are considerably increased in heart insufficiency. Intracardiac pressure and atrial and ventricular wall tension are the prime regulators of natriuretic peptides release from the heart. ANP primarily reflects atrial, and BNP ventricular overload. The in vitro stabilities of NT-proANP, BNP and NT-proBNP in EDTA whole blood are sufficient for routine determination. Specific immunochemical tests with acceptable precision are commercially available. However, the determinations are not standardized, which makes difficulties during the comparation of results gained by tests from different manufactures. BNP and NT-proBNP are in relation to ANP and NT-proANP, better diagnostic and prognostic markers of heart insufficiency. BNP measurement is useful for screening in high-risk population. BNP has an excellent negative predictive value for left ventricular dysfunction. It is also suitable for screening hypertensive patients for the discovery of hypertrophy or/and dysfunction of left ventriculy, as well as for risk assessment during the subacute phase of acute myocardial infarction. BNP and NT-proBNP measurement is also useful for treatment guidance and optimization of therapy in heart insufficiency. However, BNP determination cannot replace echocardiography or similar techniques, because these methods provide different information. Thus for the cardiologists natriuretic peptides determination is useful addition to the standard clinical investigation of patients with ventricular dysfunction.
A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.
