Is atrial natriuretic factor a physiological regulator of sodium excretion? A review of the evidence

Abstract

Recent debate has centered on the possible role of atrial natriuretic factor (ANF) as a physiological regulator of natriuresis. Plasma ANF rises with increased dietary sodium, during intravenous infusion of a saline load, and with change from upright to recumbent posture. Peptide secretion is proportional to atrial distension such that plasma concentrations rise 10-15 pM for each mm Hg increment in either right or left atrial pressures. ANF administered to humans in a low dose (0.75 pmol/kg/min) produces an increase in plasma concentrations within the normal range and induces natriuresis, excretion of cGMP, and suppression of renin-angiotensin-aldosterone activity. These results are consistent with a role for ANF in the physiological regulation of sodium excretion. Factors that clearly modify the natriuretic effect of ANF include volume/sodium status and renal perfusion pressure. Variations in these modifying factors may account for some of the reported inconsistencies in natriuresis observed in clinical high-ANF states such as congestive heart failure and tachycardia and in experimental circumstances including balloon-induced atrial distension in the cardiac-denervated dog. Overall, current data favor a role for ANF in the physiological regulation of sodium excretion in humans but more definitive evidence must await the advent of a specific ANF antagonist.