OVINE FETAL RESPONSE TO WATER DEPRIVATION: ASPECTS ON THE ROLE OF VASOPRESSIN

Abstract

The effect of maternal hyperosmolality as created by an acute mannitol infusion was evaluated in eight chronic sheep preparations. Fetal osmotic and haemodynamic responses were compared to those achieved during an arginine vasopressin (AVP) infusion into the fetus (approximately 400 µU/(min kg)). To assess the AVP sensitivity of the fetal kidney the urine osmolality was determined. The activity of adenylate cyclase was measured in placental cotyledons as an indicator of AVP receptors affecting water permeability. The maternal mannitol infusion induced an increase in fetal serum AVP levels from 1·18 ± 0·25 up to 13·76 ± 2·1 pg/ml. During the fetal AVP infusion the AVP levels were approximately 22 pg/ml, somewhat higher when given concurrently with a mannitol infusion to the ewe (peak value: 26·13 ± 2·80 pg/ml). Fetal heart rate increased significantly during maternal hyperosmolality while this effect was blunted by exogenous AVP given to the fetus. The AVP infusion did not affect fetal or maternal serum osmolality. During the mannitol infusion fetal serum osmolality increased to peak values which were not significantly different whether or not AVP was infused into the fetus (from 298·0 ± 0·85 to 309·0 ± 0·90, and from 297·7 ± 1·47 to 307·9 ± 0·90 mosmol/kg, respectively). Similarly, there were no differences in the effect of mannitol infusion upon fetal urine osmolality with or without AVP infusion (increments: + 149·7 ± 34·12 and + 148·7 ± 31·30 mosmol/kg, respectively). Adenylate cyclase activity in the placenta was unchanged before and after AVP stimulation. The data suggest an unresponsiveness of placental water permeability to fetal AVP infusion. We also conclude that a maximal urine osmolality was reached already at AVP levels obtained after an osmotic maternal load whereas at AVP levels more than twice as high the cardiovascular effects were still AVP dose‐dependent. © 1988 The Physiological Society