title: Fetal absorption of intra-amniotic aldosterone: effects on urine composition.
abstract: OBJECTIVE
  Amniotic fluid (AF) volume and composition are maintained by a balance of fetal fluid production and resorption. Ovine fetal resorption of peptide hormones (e.g., arginine vasopressin) from the amniotic cavity has been demonstrated, with resultant effects on fetal urine production. The present study was undertaken to determine whether intra-amniotically administered steroid hormones could be absorbed from the amniotic cavity into fetal plasma and whether intra-amniotic aldosterone administration would affect fetal renal sodium and potassium excretion.
  
  
  METHODS
  Seven singleton fetuses (132 +/- 2 days) were prepared with bladder, vascular, and amniotic cavity catheters. After a 5-day recovery period, a bolus of aldosterone was injected into the amniotic cavity. Fetuses were monitored for an additional 24 hours during which time maternal, fetal, and AF samples were collected at timed intervals.
  
  
  RESULTS
  After intra-amniotic aldosterone injection, AF aldosterone concentrations increased at 30 minutes and remained elevated for 4 hours after the aldosterone bolus. In response to increased AF aldosterone, fetal plasma aldosterone levels significantly increased by 30 minutes, peaked at 1 hour (17 +/- 4 to 758 +/- 160 pg/mL), and remained elevated for a minimum of 4 hours. Fetal urine sodium excretion significantly decreased and potassium excretion increased. Maternal plasma aldosterone levels increased significantly (25 +/- 10 to 401 +/- 56 pg/mL) but to levels below fetal values. Amniotic fluid and fetal and maternal aldosterone concentrations and fetal urine sodium and potassium excretion returned toward basal levels by 24 hours.
  
  
  CONCLUSIONS
  The steroid hormone aldosterone can be absorbed from the amniotic cavity into the fetal circulation and can alter fetal urine electrolyte excretion. These results suggest that the amniotic cavity is a potential route of in utero pharmacologic fetal therapy.
authors.affiliation: Department of Obstetrics and Gynecology, University of California Los Angeles School of Medicine, Harbor-UCLA Medical Center, Torrance 90502, USA. smann@prl.humc.edu
authors.forename: S E
authors.initials: SE
authors.lastname: Mann
authors.forename: M J
authors.initials: MJ
authors.lastname: Nijland
authors.forename: M G
authors.initials: MG
authors.lastname: Ross
mesh_terms: D000042:Absorption; D000450:Aldosterone / Q000378:metabolism*; D000650:Amnion / Q000378:metabolism*; D000818:Animals; D005260:Female; D005333:Fetus / Q000378:metabolism*; D011188:Potassium / Q000652:urine*; D011247:Pregnancy; D012756:Sheep; D012964:Sodium / Q000652:urine*
chemical_list: D000450:Aldosterone; D012964:Sodium; D011188:Potassium