[Atrial natriuretic factor: retrospective and perspectives].

Abstract

Since the hypotensive and natriuretic properties of crude cardiac extracts were first demonstrated in 1981 in the rat, the effector molecule has been isolated, purified and synthesized. The hormonal factor is produced by atrial myocytes in mammals and stored as a prohormone. Secretion mainly results from a volemic stress inducing an atrial stretch. Secretion includes a maturation step. A peptide of 28 amino-acids (ANP) is then released into the bloodstream. ANP has a half-life of a few minutes. ANP binds to specific receptors expressed at the target cell surface. B-receptors mediate the biological actions of ANP by an increase in cGMP while C-receptors are involved in clearance of the peptide. The kidney as well as the cardiovascular and endocrine systems are the main target sites for ANP. The renal effects of ANP are expressed by an enhanced diuresis and natriuresis which may result from an increased glomerular filtration rate and/or a reduced tubular reabsorption of salt and water. Renal hemodynamics may also be modified due to a renal specific vasodilator effect of ANP. The reduction of systemic blood pressure may result from changes in cardiac output and/or in peripheral vascular resistance. Several neurohumoral interactions of ANP also contribute to sustain the cardiovascular and renal effects described above. In view of these properties, ANP is of particular interest in order to understand the homeostasis of salt and water under physiological as well as or physiopathological conditions. In this regard, therapeutic prospects are intensively investigated. Finally, evolutionary perspectives are actually considered from studies in lower vertebrates.