Systemic arterial vasodilation in early pregnancy is accompanied by a compensatory rise in cardiac output and a decline in BP. This relative arterial underfilling in early pregnancy is coupled to stimulation of the renin-angiotensin-aldosterone system and hypotonicity. Arterial underfilling induces the nonosmotic stimulation of arginine vasopressin and upregulation of aquaporin 2 followed by trafficking of this water channel to the apical membrane of principal cells along the collecting ducts. In middle and late pregnancy, there also is a four-fold increase in vasopressinase, a cystine aminopeptidase produced by placental trophoblasts, which enhances the metabolic clearance of vasopressin. In the setting of preeclampsia, twins or triplets, or subclinical central diabetes insipidus, a transient diabetes insipidus may ensue from this vasopressinase-mediated degradation of N-terminal amino acids from the vasopressin molecule. Because desmopressin is already deaminated at the N-terminal, it is resistant to the effect of vasopressinase and therefore is the treatment of choice for transient diabetes insipidus of pregnancy.
