Maternal 1-deamino-8- d-arginine-vasopressin–induced sequential decreases in plasma sodium concentration: Ovine fetal renal responses

Abstract

Objective: Acute maternal plasma hypotonicity induces a reduced placental osmotic gradient that contributes to augmented maternal-to-fetal water flow. Subsequently, maternal plasma hyponatremia results in fetal plasma hyponatremia, increased fetal urinary flow, and ultimately increased amniotic fluid volume. We hypothesized that both the degree of reduction in the placental osmotic gradient and the degree of fetal plasma hyponatremia influence fetal urinary diuretic responses. To differentiate the roles of these factors, we determined fetal urinary responses to graded levels of plasma hyponatremia during a constant placental osmotic gradient. Furthermore, we sought to establish the minimum level of plasma hyponatremia necessary to facilitate an increase in fetal urine production. Study Design: Seven pregnant ewes (130 ± 2 days) were prepared with maternal and fetal vascular catheters and a fetal bladder catheter. After 6 days of recovery, fetal urinary flow and urine and plasma compositions were measured during a 2-hour control period. At 2 hours, tap water (2 L, 38°C) with a 20-g bolus of 1-deamino-8- d-arginine-vasopressin was administered to the ewe. Maternal plasma sodium concentration was decreased from control by 5 to 7, 10 to 12, and 15 to 17 mEq/L, and held at each level (levels 1, 2, and 3) for 60 minutes. Results: 1-Deamino-8- d-arginine-vasopressin administration induced sequential decreases in maternal and fetal plasma sodium concentrations (control 146.9 ± 0.5 mEq/L and 141.0 ± 0.5 mEq/L, respectively) at level 1 (140.1 ± 0.6 mEq/L and 136.7 ± 0.7 mEq/L, respectively), level 2 (132.5 ± 0.7 mEq/L and 130.6 ± 1.1 mEq/L, respectively), and level 3 (125.4 ± 1.2 mEq/L and 123.0 ± 1.5 mEq/L, respectively). The maternal-fetal placental osmolality and sodium gradients were constant at each hypotonicity level. Fetal urinary flow significantly increased in association with the degree of hyponatremia (from 0.17 ± 0.03 mL/kg/min to 0. 26 ± 0.04 mL/kg/min, 0.33 ± 0.05 mL/kg/min, and 0.38 ± 00.5 mL/kg/min at levels 1, 2, and 3, respectively). Conclusions: These results indicate the following: (1) Sequential decreases in maternal plasma tonicity result in parallel decreases in fetal plasma tonicity. (2) The fetal urinary diuretic response is highly correlated with the degree of fetal plasma hypotonicity, despite a constant placental osmotic gradient. A fetal therapeutic response (53% increase in fetal urine production) may be induced by a maternal plasma sodium concentration decrease of only 5 to 7 mEq/L. (Am J Obstet Gynecol 1999;180:82-90.)