An update on the physiology of atrial natriuretic factor.

Abstract

The atrial natriuretic factor (ANF) has pharmacological actions resulting in lower atrial and arterial pressures. Atrial distention stimulates ANF release, suggesting that ANF is an effector limb of a feedback loop for controlling cardiac filling pressure. To test this hypothesis it will be necessary to determine whether physiological atrial distention releases ANF in sufficient amounts to exert biological actions. Immunoblockade of endogenous ANF and attenuation of ANF release by atrial ablation inhibited volume-induced natriuresis in rats. Infusion of ANF in rats at doses mimicking those observed during experimental volume expansion produced a natriuresis sufficient to partly account for the volume-induced response. Infusion of ANF at doses expected to change plasma ANF levels minimally decreased arterial pressure in hypertensive rats over 7 days. In dogs, some studies suggest that increased plasma ANF levels following experimental changes in atrial pressure were not sufficient to exert acute cardiovascular or renal actions, whereas others support such a notion and indicate that ANF inhibited barostimulated renal renin release. This last action could alter arterial pressure in the long term by allowing sodium equilibrium at lower renal arterial pressure. Infusion of ANF in humans that produced plasma levels in the upper physiological range caused increased sodium excretion and decreased plasma renin activity. Although data are exiguous, justifying neither acceptance nor rejection of the hypothesis that ANF functions physiologically to regulate body fluid volume and arterial pressure, the current evidence slightly favors acceptance.