title: Systemic arterial vasodilation, vasopressin, and vasopressinase in pregnancy.
abstract: 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.
authors: Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA. robert.schrier@ucdenver.edu
authors: Robert W
authors: RW
authors: Schrier
mesh_terms: D010122:Cystinyl Aminopeptidase / Q000502:physiology*; D005260:Female; D006801:Humans; D011247:Pregnancy / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*; D014667:Vasopressins / Q000502:physiology*
chemical_list: D014667:Vasopressins; D010122:Cystinyl Aminopeptidase