Interaction between atrial natriuretic peptide, renin system and vasopressin in heart failure.

In heart failure, neurohumoral factors are activated, influencing ventricular performance by modulation of pre- and afterload. There is evidence from experimental models of congestive heart failure that in the early phase of the disease the sympathetic nervous system and atrial natriuretic peptide secretion are activated. Despite a reduction in cardiac output, decreased blood pressure and stimulated sympathetic nerve activity, atrial natriuretic peptide seems to be able to significantly suppress the renin-angiotensin-aldosterone system. In later phases of the disease, when more profound circulatory impairment develops, the renin system is activated and peripheral vascular resistance increases and renal blood flow decreases. In very severe heart failure, when dilutional hyponatraemia develops, plasma levels of vasopressin are inappropriately increased by nonosmolar stimuli. At the time the renin system is activated, there is an imbalance between vasodilator and vasoconstrictor mechanisms, favouring vasoconstriction which, completing the vicious circle, leads to deterioration of cardiac function.