Pathophysiological significance and clinical application of ANP and BNP inpatients with heart failure

Plasma levels of ANP and BNP increase in accordance with the severity of th e heart failure. In severe cases, the amount of BNP secreted surpasses that of ANP. The main secretion site of BNP is the ventricles, and that of ANP is the atria. However, ANP is also secreted from the ventricles as heart fa ilure advances, and thus the ventricles are important sites for both BNP an d ANP. It is well known that myocardial stretch is a key factor in the stim ulation of the secretion of ANP and BNP, although neurohumoral factors also play a role in the secretion mechanism. The major physiological effects of ANP and BNP are vasodilation, natriuresis, and inhibition of the renin-ang iotensin-aldosterone (RAA) and the sympathetic nervous systems; all of whic h are supposed to suppress the progression of heart failure. The inhibitory action of ANP and BNP on the RAA system has been considered to be an extra -cardiac effect. We recently reported the activation of an angiotensin-conv erting enzyme and aldosterone production in failing human hearts. ANP and B NP, however, would inhibit aldosterone production, not only in the adrenal cortex but also in cardiac tissue. ANP, and especially BNP, are useful mark ers of the heart's status during treatment for heart failure. The infusion of synthetic ANP (hANP) or BNP (Nesiritide(R)) is effective in the treatmen t of acute heart failure. In Japan, BNP occupies an important position in t he diagnosis of chronic heart failure, as ANP does in the treatment of acut e heart failure.