Maternal and fetal atrial natriuretic peptide levels at delivery from normal and growth retarded pregnancies

Abstract

Objective To determine whether circulating fetal levels of the vasodilator atrial natriuretic peptide (ANP) are reduced in pregnancies complicated by intrauterine growth retardation (IUGR). Design Prospective observational study. Setting Subjects 25 normal singleton pregnancies delivered at term by spontaneous vertex delivery (n = 16) or by elective caesarean section (n= 9), and a series of 14 singleton pregnancies complicated by IUGR. Intervention Measurement of ANP by radio-immunoassay in maternal venous, umbilical artery, and umbilical vein plasma from a series of normal, and IUGR pregnancies. Main outcome measures Comparison of plasma ANP levels between the three groups; relation between fetal ANP, Po, and pH. Results Mode of delivery did not influence either maternal, umbilical artery or umbilical vein plasma A N P levels in normal term singleton pregnancies. Umbilical vein ANP levels were significantly higher in the I U G R group when compared with normal pregnancies at term (mean 66 95%, CI 36-122 vs mean 37, 95% C I 29-47 pgiml, P = 0.03) and were inversely related to umbilical artery p H (R2 = 65%;Conclusions These data suggest that umbilical vein ANP levels are elevated in pregnancies complicated by IUGR, and rise appropriately in response to the stress of acidosis. In the absence of any receptor or second messenger defect within fetoplacental vascular smooth muscle, these data suggest that ANP is not directly implicated in the vascular pathophysiology of IUGR.University teaching hospital and research laboratory.

The control of blood flow to the placenta

“…However, both are weak constrictors of stem villous arteries (Maigaard, Forman & Andersson, 1986a) and are unlikely to play a major role in the control of fetoplacental vascular tone. (Kingdom, McQueen, Connell & Whittle, 1992). It has been suggested that this could represent a protective mechanism to increase blood flow in response to stress or acidosis.…”

Ultrasonographic and Biochemical Markers of Human Fetal Cardiac Dysfunction in Placental Insufficiency

“…29 There is no significant transplacental passage of NT-proANP, and mode of delivery does not influence UA plasma ANP concentrations. 4,30 In addition, atrial natriuretic factor concentrations do not change with gestation. 31 Gestational age at delivery and mode of delivery do not affect newborn cTnT levels, at least after 27 weeks' gestation.…”

Control of the fetoplacental circulation

“…46 However a more recent study suggests that umbilical vein endothelial cells may themselves synthesize ANP. 48 A similar concentration of ANP has been shown to antagonize the vasoconstrictor effects of angiotensin II in the perfused cotyledon 49 suggesting that it has a role in promoting smooth muscle relaxation under resting conditions. 48 A similar concentration of ANP has been shown to antagonize the vasoconstrictor effects of angiotensin II in the perfused cotyledon 49 suggesting that it has a role in promoting smooth muscle relaxation under resting conditions.…”

“…However perfusion of human placental cotyledons under hypoxic and acidotic conditions failed to demonstrate increased release of ET-1 into the fetal venous perfusate. 48 Functional (guanylate cyclasecoupled) vascular receptor expression for ANP in fetoplacental vessels is actually increased, as compared with gestationally-matched control placentae, in pregnancies complicated by IUGR with AEDFV in the umbilical circulation. Fetal plasma levels of renin 103 -104 and angiotensin JJIO5,IO6 m a y jj e e i e vated in cord venous blood in some cases of IUGR.…”