Atrial natriuretic factor in pregnancy and pregnancy-induced hypertension

Abstract

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.(ABSTRACT TRUNCATED AT 250 WORDS)

Peripartal Temporal Course of Endothelin 1, Angiotensin II, and Atrial Natriuretic Peptide in Pre-Eclampsia and Normotensive Pregnancy

“…This is in accordance with previous studies [13][14][15][16]. The increased ANP levels are most probably due to an increased secretion, since metabolic clearance is normal [1]. Production of ANP may be stimulated by an overloaded ventricle, increased ET-1 levels, or by fetal production [1,15].…”

“…The increased ANP levels are most probably due to an increased secretion, since metabolic clearance is normal [1]. Production of ANP may be stimulated by an overloaded ventricle, increased ET-1 levels, or by fetal production [1,15]. The action of ANP, i.e., promotion of diuresis, shift of the plasma volume to the interstitial space, and decrease in renin and aldosterone secretion, may lead to the paradoxical situation of hyporeninism, hypo-aldosteronism with hypovolaemia, and expansion of interstitial fluid volume due to increased capillary permeability [1,3].…”

“…At late pregnancy, plasma volume rises by about 1.5 litres, whereas arterial blood pressure does not exceed prepregnancy values. This suggests that vasodilation occurs [1,2]. Pre-eclampsia is characterized by a reduced expansion of plasma volume, exaggerated interstitial fluid, and an increase in blood pressure, indicating peripheral vasconstriction [1,3].…”

“…Fetal Diagn Ther 1998; 13:309-314 Zunker/Happe/Louwen/Evers/Ringelstein pressure during pregnancy has been discussed in many studies [1,[4][5][6][7][8][9][10][11][12][13][14][15][16].…”

“…It is well established that sensitivity to ANG II is increased in pregnancy-induced hypertensive disorders [12,19]. An imbalance in the production of the vasodilating prostacyclin (prostaglandin I 2 ) and the vasoconstricting thromboxane A 2 is often thought to be responsible for this [1]. However, this imbalance is not consistently found [20].…”