Pregnancy induces cardiovascular adaptations in response to increased volume overload. Aside from the hemodynamic changes that occur during pregnancy, the maternal heart also undergoes structural changes. However, cardiac modulation in pregnancies complicated by
gestational hypertension is incompletely understood. The objectives of the current investigation were to determine the role of the
natriuretic peptide (NP) system in pregnancy and to assess alterations in pregnancy-induced
cardiac hypertrophy between gestationally hypertensive and normotensive dams. Previously we have shown that mice lacking the expression of atrial NP (
ANP;
ANP(-/-)) exhibit a gestational hypertensive phenotype. In the current study, female
ANP(+/+) and
ANP(-/-) mice were mated with
ANP(+/+) males. Changes in cardiac size and weight were evaluated across pregnancy at Gestational Days 15.5 and 17.5 and Postnatal Days 7, 14, and 28. Nonpregnant mice were used as controls. Physical measurement recordings and histological analyses demonstrated peak
cardiac hypertrophy occurring at 14 days postpartum in both
ANP(+/+) and
ANP(-/-) dams with little to no change during pregnancy. Additionally, left ventricular expression of the renin-angiotensin system (RAS) and NP system was quantified by real-time quantitative polymerase chain reaction. Up-regulation of Agt and AT(1a) genes was observed late in pregnancy, while
Nppa and
Nppb genes were significantly up-regulated postpartum. Our data suggest that pregnancy-induced
cardiac hypertrophy may be influenced by the RAS throughout gestation and by the NP system postpartum. Further investigations are required to gain a complete understanding of the mechanistic aspects of pregnancy-induced
cardiac hypertrophy.