Atrial natriuretic factor in pregnancy and pregnancy-induced hypertension
Authors: Fournier Albert , Gregoire I. , Esper N. El , Lalau J. D. , Westeel P. F. , Makdassi R. , Fievet P. , de Bold A. J. 
Published: April 2011

In normal pregnancy, cross-sectional clinical data do not consistently show plasma ANF concentration differences between early pregnancy and the nonpregnant state. Sequential data in the baboon (but not in rat) show a significant decrease in plasma ANF concentration and in cardiac filling pressures in early pregnancy. The latter data support the view that pregnancy is an underfill state secondary to a primary vasodilatation. Cross-sectional and longitudinal studies in normal pregnancy in humans show that plasma ANF levels tend rise to values that are, in the third trimester, higher than in the nonpregnant state. However, late postpartum sequential data (1.5–3 months) in humans do now show a significant drop in plasma ANF concentrations, suggesting that plasma ANF is not actually increased in normal pregnancy. In the baboon (but not in the rat) there is a steady rise in plasma ANF levels to values that are significantly higher in third trimester than before pregnancy. These data suggest that in human pregnancy, in contrast with the baboon, the plasma volume expansion induced by normal pregnancy is not sensed as such by the atria probably because of an isopressive adaptation of plasma volume to an enlarged vascular bed. However, acute decrease or increase of venous return induced by low sodium diet, changing position or infusion of isotonic saline are sensed as such by the atria in normal pregnancy as in the nonpregnant state. In humans and rats, a steady rise in plasma ANF concentration is observed during the first few days after delivery suggesting that at this time the atria sense an effective hypervolemia; the latter occurring through a decrease in the functional size of the intravascular compartment owing to the elimination of the placenta as well as by the autotransfusion carried out by the emptied uterus. The resulting increase in central venous pressure may stimulate ANF release that, together with a decrease in renin and aldosterone secretion, may thus contribute to the diuretic crisis observed after delivery. In pregnancy-induced hypertension, plasma ANF levels are usually increased but may remain normal in mild hypertension. In preeclampsia, plasma ANF concentration is more consistently increased, specially in the severe form. Plasma ANF decreases to normal levels after delivery when hypertension has disappeared. Plasma ANF concentration is directly correlated to blood pressure. A deficiency in ANF secretion can not, therefore, be the primary cause of pregnancy-induced hypertension or preeclampsia. On the contrary, ANF may play a compensatory role preventing further increase of blood pressure. However, because of the suppressive effect of ANF on renin and aldosterone secretion and by promoting a shift of the plasma fluid into the interstitial space, ANF elevation in preeclampsia may actually contribute to worsen the hypovolemia and explain the paradoxical association of hypovolemia with the hypostimulation of the renin–aldosterone system. The mechanism underlying the increased ANF secretion in preeclampsia is not clear since cardiac filling pressures in untreated preeclampsia are decreased and hence increased ANF release through atrial stretch seems unlikely. It is possible that neuroendocrine mechanisms yet to be identified are responsible for this observation.Key words: atrial natriuretic factor, pregnancy, preeclampsia, pregnancy-induced hypertension.