Abstract
The fetus appears to be capable of homeostatic regulation of its fluid environment in utero. Possible hormonal modulation mechanisms influencing cardiovascular homeostasis include AVP, which in adult animals is released from the posterior pituitary in response to hyperosmolar stimuli or volume depletion. Fetal AVP production was studied in chronically prepared unstressed fetuses and in acutely hemorrhaged fetuses from 0.4 of gestation to term. Serum levels of AVP were measured by specific radioimmunoassay. Assay cross reactivity with fetal arginine vasotocin and angiotension 1 was negligible. In chronically catheterized fetuses, basal AVP levels rose from 0 pg/ml at gestation age (GA) 112d to 2.4 pg/ml (5mU/ml) at GA 140d. Epidural anesthesia to the ewe and acute catheterization of the fetus was associated with mean fetal levels of 14.9 pg/ml. In these fetuses, sequential hemorrhage of 5 to 20% of total blood volume resulted in an increase of serum AVP. Mean AVP levels for 4 fetuses 130-148 GA were 48.1 pg/ml after 5% bleeding, 200.1 pg/ml after 10%. 106 pg/ml after 15% and 151 pg/ml after 20%. A very early gestation fetus (GA 59) had a higher basal level after anesthesia and exteriorization: 56.8 pg/ ml. This increased only to 69.1 pg/ml after 10% hemorrhage. That such a large release of this membrane active hormone is present early in gestation when the kidneys are extremely immature, suggests that AVP may act to control water metabolism at membrane surfaces other than renal in the fetal placental unit. Supported by USPHS Grant HL 06285.
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Drummond, W., Rudolph, A., Keil, L. et al. ARGININE VASOPRESSIN (AVP) IN FETAL LAMBS & RESPONSE TO BLOOD LOSS. Pediatr Res 11, 405 (1977). https://doi.org/10.1203/00006450-197704000-00213
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DOI: https://doi.org/10.1203/00006450-197704000-00213