Compensatory mechanisms underlying arginine vasopressin regulation in transient polyuria during pregnancy

Transient polyuria during pregnancy is reportedly caused by increased arginine vasopressin (AVP) degradation due to vasopressinase produced by the placenta. The mechanism underlying transient polyuria during pregnancy has not been established. In this study we measured urine volume, urine osmolality, and AVP transcriptional activity during pregnancy in wild-type and familial neurohypophysial diabetes insipidus (FNDI) mice. The FNDI mice were used as a partial AVP deficiency model. Vasopressinase was shown to be present in the placentas of pregnant mice. The Avp hnRNA level in the supraoptic nucleus, which is indicative of AVP transcriptional activity, was upregulated in wild-type and FNDI mice during late pregnancy. FNDI mice, but not wild-type mice, had a significant increase in urine volume and a decrease in urine osmolality during pregnancy. These data suggest that an increase in urine volume during pregnancy only occurs when the compensatory increase in AVP release is insufficient to counteract degradation by vasopressinase. • AVP transcriptional activity was upregulated in pregnant WT and FNDI mice. • There were no urine volume or osmolality changes in WT mice during pregnancy. • Urine volume increased and osmolality decreased in FNDI mice during pregnancy. • Polyuria worsened in pregnant FNDI mice due to deficient AVP degradation compensation.