title: The roles of arginine vasopressin in fetal sodium balance and as a mediator of the effects of fetal "stress".
abstract: To see if arginine vasopressin (AVP) influenced fetal sodium balance, we infused AVP i.v. (45 mU h-1 kg-1) into two groups of chronically catheterized fetal sheep. One group had urinary osmolalities of 147 +/- 23 mosm kg-1 (SEM, n = 6) and the other group had higher urinary osmolalities (339 +/- 3 mosm kg-1, n = 4, P < 0.001). The group with high urinary osmolalities had higher systolic pressures (P < 0.05), higher glomerular filtration rates (GFR; P < 0.05), and higher urinary electrolyte excretion rates (P < 0.05), but lower membrane blood flows (P < 0.05) and lower fractional reabsorption of sodium by the proximal tubule (P < 0.01). In the group with low urinary osmolalities, AVP caused a rise in arterial blood pressure (P < 0.001), a fall in heart rate (P < 0.001), a fall in membrane blood flow (P < 0.02), but no change in placental or renal blood flow. Renal sodium excretion increased (P < 0.001) because GFR rose (P < 0.001) and proximal fractional sodium reabsorption fell (P < 0.001). Distal fractional sodium reabsorption increased (P < 0.001), but not enough to compensate for the fall in proximal fractional reabsorption. Lung liquid flow decreased (P = 0.006), as did lung liquid sodium excretion (P = 0.002). There were no changes in fetal plasma sodium, blood volume or haematocrit. The effects of AVP infusion were similar in the group with high urinary osmolalities. This study shows that high levels of AVP, such as occur in fetal "stress", have widespread effects on fetal cardiovascular, renal and lung functions. The characteristic profile of the fetuses with high urinary osmolalities prior to AVP infusion could be entirely explained by high endogenous AVP levels and AVP could possibly be a sole mediator of these widespread effects of fetal "stress". Furthermore, although during infusion of AVP sodium excretion increased, blood volumes did not change. Therefore, the fetuses must have accessed additional sodium from either their extracellular fluids, the amniotic and/or allantoic cavities or across the placenta.
authors.affiliation: School of Physiology and Pharmacology, University of New South Wales, Kensington, Australia.
authors.forename: K J
authors.initials: KJ
authors.lastname: Gibson
authors.forename: E R
authors.initials: ER
authors.lastname: Lumbers
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology*; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000187:drug effects; D001810:Blood Volume; D004573:Electrolytes / Q000097:blood; D005260:Female; D005315:Fetal Diseases / Q000378:metabolism; D005333:Fetus / Q000378:metabolism*; D006340:Heart Rate, Fetal / Q000187:drug effects; D006400:Hematocrit; D006863:Hydrogen-Ion Concentration; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D009994:Osmolar Concentration; D011247:Pregnancy; D012756:Sheep; D012964:Sodium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D013312:Stress, Physiological / Q000378:metabolism; D014882:Water-Electrolyte Balance / Q000187:drug effects
chemical_list: D004573:Electrolytes; D001127:Arginine Vasopressin; D012964:Sodium