Impairment of cardiac natriuretic peptide signaling develops the excessive cardiac hypertrophy during lactation period. Mus musculus

Two natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) act through the common receptor, guanylyl cyclase-A (GC-A) to lower blood pressure, induce diuresis/natriuresis and dilate blood vessels. Recently, we discovered that the excessive cardiac hypertrophy accompanied with cardiac dysfunction was induced in the lactating natriuretic peptide receptor 1 (Npr1, which encodes GC-A)-deficient mice. To clarify the cause of lactation-induced cardic hypertrophy in Npr1-/-, we performed the gene expressions analysis using nulliparous (NP) or postpartum lactating wild-type (Npr1+/+) and Npr1-/- mice. Numerous genes were altered in the postpartum lactating period both in Npr1+/+ and Npr1-/-. Additionally, the involvement of inflammatory responce in the cardiac hypertrophy in lactating-Npr1-/- mice was clarified bythe gene ontology analysis. Overall design: Gene expressions of female mice heart were examined in nulliparous (NP) and lactating (Lactation) Npr1+/+ and Npr1-/- mice. Four independent mice were utilized for analysis.