[Renin, aldosterone and prostaglandins in heart failure]

In heart failure, neurohumoral factors are important determinants of left-ventricular function, not only by direct mechanisms on the myocardium, but also by indirect effects through modulation of pre- and afterload. In experimental models of heart failure, as well as in patients with cardiac dysfunction, it has been demonstrated in the early phase of the disease that the sympathetic activity and the secretion of atrial natriuretic peptide are stimulated. This is associated with an increased synthesis of vasodilator prostaglandins in the kidney, predominately prostaglandin E2. Prostaglandin E2 plays an important role by its vasodilator and natriuretic properties in preserving renal blood flow, natriuresis and diuresis. The stimulation of the secretion of atrial natriuretic peptide in relatively moderate heart failure leads to a suppression of the activation of the renin-angiotensin-aldosterone system. In more severe heart failure vasoconstrictor, sodium and water-retaining mechanisms like the renin-angiotensin-aldosterone system are activated with the consequence of an increase of systemic vascular resistance, a reduction of renal blood flow, and an increased fluid retention. The inhibition of cyclooxygenase, leading to a blockade of the synthesis of prostaglandins, leads in early heart failure to a dramatic change in renal blood flow with an increase of renal vascular resistance and a decrease of renal perfusion which causes renal functional impairment.