Atrial Natriuretic Peptide and Hemodynamic Changes During Normal Human Pregnancy

Abstract

Abstract We compared plasma atrial natriuretic peptide (ANP) and cGMP levels during normal pregnancy—a condition characterized by hypervolemia, high cardiac output, and decreased vascular resistance—with postpartum levels and assessed their relation to pregnancy-induced hemodynamic changes. Humoral and hemodynamic variables were measured in healthy women subjects in the supine and upright postures at each trimester of pregnancy and postpartum. Supine plasma ANP was increased throughout pregnancy (32±5, 21±3, and 19±2 versus 15±1 pmol · L −1 , respectively, at each trimester versus postpartum), as was cGMP (8.6±1, 7.1±1, and 6.6±1 versus 5.6±1 nmol · L −1 ), and their increments were directly related ( r =.68, P <.01). Both ANP and cGMP levels did not differ from postpartum levels after subjects stood. Supine stroke volume was initially increased but declined below postpartum levels in late pregnancy (69±4, 60±3, and 44±3 versus 58±4 mL · m −2 ), whereas after subjects stood it was always higher (56±3, 58±3, and 49±2 versus 44±2 mL · m −2 ); thus, stroke volume tended to increase in response to standing in late pregnancy. Supine cardiac index had a similar trend, which was opposite to that of total peripheral resistance (1213±62, 1265±79, and 1729±89 versus 1654±92 dyne · s −1 · cm −5 · m −2 ). The increments of supine ANP throughout pregnancy were directly related to the changes of stroke volume ( r =.40, P <.01), and those of cGMP were inversely related to the changes of total peripheral resistance ( r =−.46, P <.01). We conclude that in early pregnancy ANP secretion is stimulated by hypervolemia, which also increases stroke volume. In late pregnancy, these changes in the supine position wear off because of the impairment of venous return by the pregnant uterus, which is relieved after standing. The increased plasma ANP may contribute to the systemic vasodilation during pregnancy, and this effect is mediated by its second messenger cGMP.