DDAVP-induced maternal hyposmolality increases ovine fetal urine flow

1995 ◽  
Vol 268 (2) ◽  
pp. R358-R365 ◽  
Author(s):  
M. J. Nijland ◽  
M. G. Ross ◽  
L. K. Kullama ◽  
K. Bradley ◽  
M. G. Ervin
Keyword(s):  
Tap Water ◽  
Control Period ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Maternal Plasma ◽  
Urine Flow ◽  
Fetal Plasma ◽  
Maternal Urine ◽  
Fetal Urine ◽  
Fluid Transfer

Fetal urine flow is influenced by fetal intravascular volume, glomerular filtration rate, tubular reabsorption, and fluid regulatory hormones. As maternal-to-fetal fluid transfer is dependent on hydrostatic and osmotic gradients, we postulated that a chronic decrease in maternal plasma osmolality would promote transplacental fluid transfer and increase fetal urine flow. Six pregnant ewes and singleton fetuses (131 +/- 2 days; term = 150 days) received bladder and hindlimb arterial and venous catheters. After 5 days, plasma and urine composition, urine flow rate (Uvol), and plasma arginine vasopressin (AVP) levels were measured during a 2-h control period. At 2 h, tap water (2 liter, 38 degrees C) was administered to the ewe. At 3 h, ewes received a 20-micrograms bolus of 1-desamino-[D-Arg8]vasopressin (DDAVP), followed by continuous infusion (4 micrograms/h). In response to water loading, maternal urine osmolality decreased (761 +/- 158 to 339 +/- 13 mosmol/kgH2O), and Uvol increased. After DDAVP, maternal urine osmolality increased (1,270 +/- 89 mosmol/kgH2O), and Uvol, hematocrit, plasma osmolality (304 +/- 1 to 284 +/- 4 mosmol/kgH2O), and protein concentration decreased. Five hours after maternal DDAVP infusion, fetal plasma osmolality decreased (300 +/- 1 to 281 +/- 3 mosmol/kgH2O), and Uvol increased (0.4 +/- 0.1 to 1.3 +/- 0.2 ml/min) and remained elevated at 24 h. There was no change in fetal plasma DDAVP (immunoreactive AVP) levels or fetal urine osmolality. Controlled changes in maternal plasma osmolality may prove useful in modulating fetal urine flow and, ultimately, amniotic fluid volume.

Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume

1996 ◽  
Vol 81 (6) ◽  
pp. 2588-2594 ◽  
Author(s):  
Stephanie E. Mann ◽  
Mark J. M. Nijland ◽  
Michael G. Ross
Keyword(s):  
Amniotic Fluid ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Fluid Volume ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Amniotic Fluid Volume ◽  
Fetal Urine ◽  
Ovine Fetal

Mann, Stephanie E., Mark J. M. Nijland, and Michael G. Ross.Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume. J. Appl. Physiol. 81(6): 2588–2594, 1996.—Adequate amniotic fluid (AF) volume is maintained by a balance of fetal fluid production (lung liquid and urine) and resorption (swallowing and intramembranous flow). Because fetal urine is the principle source of AF, alterations in urine flow and composition directly impact AF dynamics. Intra-amniotic 1-desamino-8-d-arginine vasopressin (DDAVP) is rapidly absorbed into fetal plasma and induces a marked fetal urinary antidiuresis. To examine the effect of intra-amniotic- DDAVP-induced fetal urinary responses on AF volume and composition, six chronically prepared ewes with singleton fetuses (gestation 128 ± 2 days) were studied for 72 h after a single intra-amniotic DDAVP (50-μg) injection. After DDAVP, fetal urine osmolality significantly increased at 2 h (157 ± 13 to 253 ± 21 mosmol/kg) and remained elevated at 72 h (400 ± 13 mosmol/kg). Urinary sodium (33.0 ± 4.5 to 117.2 ± 9.7 meq/l) and chloride (26.0 ± 2.8 to 92.4 ± 8.1 meq/l) concentrations similarly increased. AF osmolality increased (285 ± 3 to 299 ± 4 mosmol/kgH2O), although there was no change in fetal plasma osmolality (294 ± 2 mosmol/kg). Despite a 50% reduction in fetal urine flow (0.12 ± 0.03 to 0.05 ± 0.02 ml ⋅ kg−1 ⋅ min−1at 2 h and 0.06 ± 0.01 ml ⋅ kg−1 ⋅ min−1after 72 h), AF volume did not change (693 ± 226 to 679 ± 214 ml). There were no changes in fetal arterial blood pressures, pH,[Formula: see text], or[Formula: see text] after DDAVP. We conclude the following. 1) Intra-amniotic DDAVP injection induces a prolonged decrease in fetal urine flow and increases in urine and AF osmolalities. 2) Despite decreased urine flow, AF volume does not change. We speculate that, in response to DDAVP-induced fetal oliguria, reversed intramembranous flow (from isotonic fetal plasma to hypertonic AF) preserves AF volume.

Fetal diuretic responses to maternal hyponatremia: contribution of placental sodium gradient

1999 ◽  
Vol 87 (4) ◽  
pp. 1440-1447 ◽  
Author(s):  
Todd J. Roberts ◽  
Mark J. M. Nijland ◽  
Leslee Williams ◽  
Michael G. Ross
Keyword(s):  
Blood Volume ◽  
Tap Water ◽  
Maternal Plasma ◽  
Urine Flow ◽  
Fetal Blood ◽  
Fetal Plasma ◽  
Sodium Gradient ◽  
Fetal Urine ◽  
Diuretic Response ◽  
Absolute Decrease

Maternal hyponatremia induces fetal hyponatremia and increased fetal urine flow. We sought to examine the relative contributions of the placental Na+gradient vs. the absolute decrease in fetal plasma Na+ in the fetal diuretic response to hyponatremia. Seven ewes with singleton fetuses (130 ± 2 days) were prepared. Ewes received intravenous 1-desamino-8-d-arginine vasopressin (20 μg) and warm tap water (2 liters). Maternal plasma Na+ was decreased to achieve two levels of maternal hyponatremia. Maternal and fetal blood volume were measured with radiolabeled red blood cells. In response to the first decrease in maternal plasma Na+, fetal plasma Na+ did not change initially. Subsequently, fetal plasma Na+ decreased, normalizing the gradient. The second decrease in maternal plasma Na+ similarly induced a reduced and normalized placental gradient at lower fetal plasma Na+ values. Fetal urine flow increased in direct proportion to the degree of fetal hyponatremia (13, 38, 63, 100%, respectively). Maternal, although not fetal, blood volume significantly increased in response to hyponatremia. These results suggest that chronic fetal hyponatremia will result in a persistent diuresis, despite placental equilibration.

Maternal/fetal dehydration: prolonged effects and responses to oral rehydration

1993 ◽  
Vol 264 (1) ◽  
pp. R197-R203 ◽  
Author(s):  
C. L. Agnew ◽  
M. G. Ross ◽  
Y. Fujino ◽  
M. G. Ervin ◽  
L. Day ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Plasma Osmolality ◽  
Maternal Plasma ◽  
Urine Flow ◽  
Fetal Blood ◽  
Water Access ◽  
Oral Rehydration ◽  
Fetal Plasma ◽  
Plasma Arginine

Dehydration induces marked alterations in maternal-fetal fluid homeostasis and accompanying fetal endocrine responses. We sought to determine if the increase in fetal plasma arginine vasopressin (AVP) levels during maternal dehydration is mediated by fetal plasma hypovolemia in addition to hyperosmolality and to examine maternal and fetal plasma atrial natriuretic factor (ANF) responses to maternal dehydration and oral rehydration. Seven pregnant ewes (127 +/- 1 day) were water deprived for 72-96 h, and five of these were orally rehydrated. Dehydration induced significant increases in maternal plasma osmolality (pOSM) (300 +/- 2 to 325 +/- 8 mosmol/kg) and AVP (3.0 +/- 0.4 to 18.9 +/- 4.0 pg/ml), and decreases in plasma ANF levels (28.1 +/- 3.1 to 19.7 +/- 3.1 pg/ml). Fetal pOSM (293 +/- 3 to 314 +/- 4 mosmol/kg), AVP (2.5 +/- 0.6 to 8.1 +/- 4.8 pg/ml), and urinary fractional sodium excretion increased significantly, whereas plasma ANF and fetal blood volume did not change. After maternal water access maternal plasma AVP decreased rapidly in comparison to the gradual decrease in maternal pOSM. Fetal plasma AVP levels did not change significantly and fetal pOSM decreased more slowly than maternal pOSM. Fetal plasma ANF increased in association with increased urine flow and glomerular filtration rate after maternal rehydration. These data indicate marked differences in fetal and maternal plasma ANF and AVP responses with dehydration-induced increases in fetal plasma AVP being secondary to plasma hyperosmolality, rather than hypovolemia. Rapid suppression of maternal plasma AVP may contribute to the slower equilibration of fetal pOSM during oral, as compared with intravenous, maternal rehydration.

Role of arginine vasopressin in fetal renal response to hypertonicity

1986 ◽  
Vol 251 (1) ◽  
pp. F156-F163
Author(s):  
L. L. Woods ◽  
C. Y. Cheung ◽  
G. G. Power ◽  
R. A. Brace
Keyword(s):  
Renal Function ◽  
Arginine Vasopressin ◽  
Urine Osmolality ◽  
Maternal Blood ◽  
Urine Flow ◽  
Fetal Blood ◽  
Fetal Plasma ◽  
Fetal Urine ◽  
Sustained Increase

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.

Fetal renal contribution to amniotic fluid osmolality during maternal hypertonicity

1986 ◽  
Vol 250 (2) ◽  
pp. R235-R239
Author(s):  
L. L. Woods
Keyword(s):  
Amniotic Fluid ◽  
Continuous Infusion ◽  
Arginine Vasopressin ◽  
Urine Osmolality ◽  
Uterine Wall ◽  
Urine Flow ◽  
Bulk Flow ◽  
Vasopressin Antagonist ◽  
Fetal Plasma ◽  
Fetal Urine

The contribution of fetal urine to the increase in amniotic fluid osmolality during maternal hypertonicity was studied in chronically catheterized sheep of 130-135 days gestation. Nine percent NaCl was injected simultaneously into fetal and maternal veins, followed by a continuous infusion into the maternal vein. Maternal and fetal plasma osmolalities rose by 15 +/- 1 (SE) and 13 +/- 1 mosmol/kg, respectively, and remained constant for 4 h. Fetal urine osmolality rose significantly from 188 +/- 31 to 277 +/- 32 mosmol/kg within 1 h and remained constant thereafter. Fetal urine flow rose transiently, fell to normal within 10 min, and averaged 70% of normal beyond 1 h. Amniotic fluid osmolality rose by 10.8 +/- 2.8 mosmol/kg over 4 h. Following hypertonic injection into three fetuses blocked by the arginine vasopressin antagonist d(CH2)5D-tyr(Et)VAVP, urine osmolality did not change, and amniotic fluid osmolality rose by 2.7 +/- 0.3 mosmol/kg. Thus it appears that the increase in amniotic fluid osmolality during maternal hypertonicity may be due largely to an increased fetal urine osmolality coupled with a decreased flow of fetal urine into the amniotic space, rather than to bulk flow of fluid across the membranes and uterine wall.

Maternal DDAVP-induced hyponatremia preserves fetal urine flow during acute fetal hemorrhage

2003 ◽  
Vol 285 (2) ◽  
pp. R373-R379 ◽  
Author(s):  
Mina Desai ◽  
Zhice Xu ◽  
Catalina Guerra ◽  
Nathash Kallichanda ◽  
Michael G. Ross
Keyword(s):  
Amniotic Fluid ◽  
Tap Water ◽  
Plasma Osmolality ◽  
Cardiovascular Responses ◽  
Urine Flow ◽  
Fluid Volume ◽  
Plasma Sodium ◽  
Amniotic Fluid Volume ◽  
Fetal Urine ◽  
The Impact

Maternal administration of DDAVP induces maternal and fetal plasma hyponatremia, accentuates fetal urine flow, and increases amniotic fluid volume. Fetal hemorrhage represents an acute stress that results in fetal AVP secretion and reduced urine flow rate. In view of the potential therapeutic use of DDAVP for pregnancies with reduced amniotic fluid volume, we sought to examine the impact of maternal hypotonicity during acute fetal hemorrhage. Chronically catheterized pregnant ewes (130 ± 2 days) were allocated to control or to DDAVP-induced hyponatremia groups. In the latter group, tap water (2,000 ml) was administered intragastrically to the ewe followed by DDAVP (20 μg bolus, 4 μg/h) and a maintenance intravenous infusion of 5% dextrose water for 4 h to achieve maternal hyponatremia of 10–12 meq/l. Thereafter, ovine fetuses from both groups were continuously hemorrhaged to 30% of estimated blood volume over a 60-min period. DDAVP caused similar degree of reductions in plasma sodium and osmolality in pregnant ewes and their fetuses. In response to hemorrhage, DDAVP fetuses showed greater reduction in hematocrit than control fetuses (14 vs. 10%). Both groups of fetuses demonstrated similar increases in plasma AVP concentration. However, the AVP-hemorrhage threshold was greater in DDAVP fetuses (22.5%) than in control (17.5%). Hemorrhage had no significant impact on plasma osmolality, electrolyte levels, or cardiovascular responses in either group of fetuses. Despite similar increases in plasma AVP, DDAVP fetuses preserved fetal urine flow rates, with values threefold those of control fetuses. These results suggest that under conditions of acute fetal stress of hemorrhage, maternal DDAVP may preserve fetal urine flow and amniotic fluid volume.

Fetal-maternal fluid and electrolyte relations during chronic fetal urine loss in sheep

1992 ◽  
Vol 263 (4) ◽  
pp. F671-F679 ◽  
Author(s):  
M. E. Wlodek ◽  
R. Harding ◽  
G. D. Thorburn
Keyword(s):  
Phase 1 ◽  
Plasma Osmolality ◽  
Chronic Phase ◽  
Allantoic Fluid ◽  
Maternal Plasma ◽  
Late Gestation ◽  
Control Group ◽  
Osmotic Gradient ◽  
Fetal Plasma ◽  
Fetal Urine

Our aim was to determine the effects of prolonged removal of fetal urine during late gestation on fetal-maternal fluid and electrolyte relationships. We measured the volume and composition of fetal urine and amniotic and allantoic fluids and the composition of fetal and maternal plasma in sheep before and during continuous urine drainage, which began at 130 days of gestation and continued until the onset of labor; a control group was also studied. The response to fetal urine drainage occurred in two phases. In the "acute" phase (1-3 days), amniotic and allantoic fluid volumes decreased significantly, presumably due to their reabsorption into the fetal chorionic circulation or swallowing of amniotic fluid by the fetus. During the "chronic" phase, starting 3-5 days after urine drainage, a significant reversal in the transplacental osmotic gradient occurred due to a decrease in maternal plasma osmolality. During the entire drainage period (14.1 +/- 1.1 days, mean +/- SE, n = 5) at least 542 ml/day of water and 24 mmol/day of electrolytes passed from the mother into the fetal circulation and fetal plasma osmolality was unchanged. We conclude that, despite the loss of substantial water and electrolytes, the fetus is able to maintain its growth and fluid and electrolyte homeostasis by obtaining water and electrolytes initially from the amniotic and allantoic fluids and subsequently from its mother. The movement of water and electrolytes to the fetus would have been facilitated by the reversed transplacental osmotic gradient.

Intraruminal rehydration of ovine fetuses

1991 ◽  
Vol 261 (6) ◽  
pp. R1381-R1387
Author(s):  
M. G. Ross ◽  
D. J. Sherman ◽  
M. G. Ervin ◽  
L. Day
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Distilled Water ◽  
Intravascular Volume ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Po2

During oral rehydration of adult mammals, oropharyngeal stimulation, the act of swallowing, and/or gastric factors contribute to a rapid decrease in plasma arginine vasopressin (AVP) that precedes plasma osmolality changes. To determine whether similar mechanisms are present in the developing fetus, six chronically prepared ovine fetuses were rehydrated with intraruminal (IR) distilled water infusions (1 ml.kg-1.min-1 for 60 min) after 43 +/- 3 h of maternal water deprivation. In response to maternal dehydration, significant increases were noted in maternal and fetal mean plasma osmolalities, sodium and AVP concentrations, and fetal urine osmolality. As estimated by hematocrit, fetal intravascular volume decreased by 11%. Fetal rehydration via IR distilled water infusion evoked a significant decrease in fetal plasma osmolality but no change in urine osmolality. Unexpectedly, fetal arterial blood pressure increased and arterial PO2 decreased while fetal hematocrit indicated a further 7% decrease in intravascular volume after the IR infusion. There was a nonsignificant trend toward increased fetal glomerular filtration rate, urine volume, and plasma AVP concentrations. Identical IR water infusions to five euhydrated fetuses resulted in significant decreases in fetal plasma osmolality and increases in glomerular filtration rate, urine flow, and osmolar excretion. The euhydrated fetuses also exhibited significant increases in mean arterial blood pressure and hematocrit and decreased fetal arterial PO2. These results indicate that IR water does not suppress AVP secretion in the dehydrated ovine fetus. Rather, both euhydrated and dehydrated fetuses exhibit an idiosyncratic vasoconstrictive response to IR water.

Sex difference in urinary concentrating ability of rats with water deprivation

1996 ◽  
Vol 270 (3) ◽  
pp. R550-R555 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
J. Miller ◽  
C. J. Sigman ◽  
H. Liu ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Ovarian Hormones ◽  
Urine Flow ◽  
The Other ◽  
Consumptive Behavior ◽  
Urinary Concentrating Ability ◽  
Previous Demonstration

Our previous demonstration of sexual dimorphism in the antidiuretic response to exogenous vasopressin prompted us to investigate the response to moderately high levels of endogenous vasopressin stimulated by water deprivation in conscious rats. After 24 h water deprivation, urine flow was significantly higher and urine osmolality lower in females than in males. Plasma concentrations of vasopressin were higher in females than in males after water deprivation, but plasma osmolality did not differ. Gonadectomy, which had no effect in dehydrated males, decreased urine flow and increased urine osmolality in females to levels observed in intact and gonadectomized males. Spontaneous water intake was also measured and found to be lower in males and estrous females than in females in the other phases of the estrous cycle. These observations support the concept that there is a gender difference in the antidiuretic responsiveness to endogenous vasopressin, that this difference is dependent upon the ovarian hormones, and that it may lead to differences in consumptive behavior.

Maternal dehydration-rehydration: fetal plasma and urinary responses

1988 ◽  
Vol 255 (5) ◽  
pp. E674-E679 ◽  
Author(s):  
M. G. Ross ◽  
D. J. Sherman ◽  
M. G. Ervin ◽  
R. Castro ◽  
J. Humme
Keyword(s):  
Glomerular Filtration Rate ◽  
Arginine Vasopressin ◽  
Filtration Rate ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Fetal Plasma ◽  
Urine Production ◽  
The Impact ◽  
Observation Period

Pregnant women may be exposed to exercise, thermal, or gastrointestinal (hyperemesis) water loss, all of which commonly induce a greater than 10 mosmol increase in plasma osmolality. Although fetal osmolality is dependent on maternal osmolality, the impact of maternal dehydration and subsequent maternal rehydration on the fetus has not been explored. Five pregnant ewes with singleton fetuses (136 +/- 1 day) were water deprived for 36 h resulting in a significant increase in plasma osmolality (298 +/- 3.4 to 313 +/- 5.0 mosmol). In response to maternal dehydration, fetal plasma osmolality (297.0 +/- 4.1 to 309.3 +/- 4.1 mosmol), arginine vasopressin (AVP) levels (1.5 +/- 0.2 to 7.9 +/- 1.0 pg/ml), hematocrit (35.1 to 38.6%), and urine osmolality (161.3 +/- 10.7 to 348.9 +/- 21.9 mosmol) significantly increased. Subsequently, ewes were rehydrated over 4 h with intravenously infused 0.45% saline (20 ml.kg-1.h-1). In response to maternal rehydration, maternal and fetal plasma osmolality decreased to basal values (298.9 +/- 3.2 and 300.1 +/- 3.8 mosmol, respectively) and fetal glomerular filtration rate (1.72 +/- 0.30 to 3.08 +/- 0.66 ml/min) and urine volume significantly increased (0.33 +/- 0.02 to 0.71 +/- 0.13 ml/min). However, fetal hematocrit (37.4%), plasma AVP (3.1 +/- 0.9 pg/ml), and urine osmolality (255.4 +/- 28.8 mosmol) did not return to basal levels during the observation period. These results demonstrate fetal hyperosmolality, blood volume contraction, AVP secretion, and altered urine production in response to maternal dehydration. Despite maternal rehydration and normalization of maternal and fetal plasma osmolality, fetal endocrine and fluid responses are prolonged.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document