We studied the effects of hyperosmolality on fetal renal function and the role of arginine vasopressin (AVP) in these responses. NaCl (9%) was injected intravenously into chronically catheterized ewes and their fetuses, followed by a continuous infusion of 9% NaCl into the ewes. The fetuses were either normal, infused with AVP, or infused with an AVP antagonist. In normal fetuses NaCl injection caused fetal and maternal blood osmolalities to be elevated by 10-15 mosmol/kg for 4 h with no change in fetal blood volume; fetal plasma AVP rose 42%. Fetal arterial pressures rose transiently by 2-10 mmHg. Fetal urine flow rose transiently by 73% after NaCl injection and then averaged 27% below control after 1 h, whereas fetal urine osmolality increased from 188 ± 31 to 282 ± 33 mosmol/kg. In a second group of fetuses AVP infusion alone caused fetal urine osmolality to increase by 123 ± 39 mosmol/kg and urine flow to fall 31%, whereas in a third group the antagonist alone had no effect on urine flow or osmolality. After hypertonic injection into fetuses infused with AVP or the antagonist, the transient changes were similar to those in normal fetuses. However, the sustained increase in urine osmolality and decrease in flow after hypertonic injection were abolished in AVP-infused and antagonist-infused fetuses. Thus it appears that the transient changes in fetal renal function after hypertonic injection are not AVP-induced and may be due to transient increases in arterial pressure, whereas the prolonged changes in urine flow and osmolality appear to be mediated by increases in fetal plasma AVP levels.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - Jan 1 1986|
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