[Conditions of secretion and peripheral effects of atrial natriuretic peptide in heart failure].

In heart failure, ventricular function is influenced by modulation of pre- and afterload. It has been shown that the secretion of atrial natriuretic peptide (ANP) is increased in experimental preparations of heart failure and in patients with cardiac failure. Distension of myoendocrine cells of the atria is the major stimulus for the release of ANP. The possible beneficial effect of ANP in heart failure consists of unloading the heart by its vasodilatory, diuretic, and natriuretic properties. Intravenous application of high, pharmacological doses of ANP improves ventricular performance by a reduction of pre- and afterload, the renal effects however, are markedly attenuated. From animal experiments one may conclude that ANP may play an important role in early and moderate heart failure as a counterregulating mechanism of the renin-angiotensin-aldosterone system. In chronic severe heart failure vasoconstrictory, volume, and sodium-retaining mechanisms override the effects of ANP, deteriorating ventricular function by an inadequate increase of pre- and afterload. The attenuation of the effects of ANP in cardiac failure may be due to altered hemodynamics especially in the kidney, to a counterregulation of vasoconstrictory and volume-retaining neurohumoral factors, to a reduction of specific binding sites for ANP (receptor "down-regulation"), and to a possible intracellular defect beyond the formation of cGMP, the intracellular second messenger of ANP.