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.

The Responses to Water Deprivation in Lithium-Treated Patients with and without Polyuria

1982 ◽  
Vol 63 (6) ◽  
pp. 549-554 ◽  
Author(s):  
D. B. Morgan ◽  
M. D. Penney ◽  
R. P. Hullin ◽  
T. H. Thomas ◽  
D. P. Srinivasan
Keyword(s):  
Water Intake ◽  
Water Deprivation ◽  
Urine Osmolality ◽  
Drug Group ◽  
Urine Flow ◽  
The Other ◽  
Control Group ◽  
Manic Depressive ◽  
Renal Concentrating Mechanism ◽  
Depressive Patients

1. Urine osmolality and plasma and urine arginine vasopressin (AVP) were measured before, during and at the end of 23 h of water deprivation in four groups of subjects. There were eight non-polyuric manic-depressive patients taking lithium (the lithium group), seven manic-depressive patients taking other psychotropic drugs but not lithium (the other drug group), seven healthy subjects (the control group) and three lithium-treated patients with polyuria (the polyuric lithium group). 2. The lithium group had a resistance to the effect of AVP on the renal tubule with a fivefold increase in AVP excretion at a given urine osmolality. However, their water homoeostasis was intact as they lost no more weight during water deprivation than did the control group. 3. The relationship beween urine osmolality and AVP excretion has been defined from these results and the effect of lithium treatment on it has been characterized. The results suggest that lithium competitively inhibits the effect of AVP on the renal concentrating mechanism but does not decrease the ‘theoretical’ maximum urine osmolality. 4. The other drug group had a high basal urine flow which was due to a primary increase in water intake. The responsiveness of the renal concentrating mechanism to AVP was the same in this group as in the control group. 5. The polyuric lithium group had the highest basal urine flow and lost the greatest amount of weight during water deprivation. Neither urine osmolality nor AVP excretion was at a maximum in the basal state, as both increased during water deprivation. These relationships between urine osmolality and AVP excretion indicated a much greater resistance to AVP than in the other lithium-treated patients. 6. We suggest that these patients are polyuric as they become thirsty and drink before their AVP secretion increases to levels high enough to overcome the resistance to AVP. The results suggest, however, that in the basal state their water intake may be more than the minimum determined by the resistance to AVP.

EFFECTS OF ARGININE-, LYSINE- AND LEUCINE-VASOPRESSIN ON URINARY OSMOLALITY AND RATE OF URINE FLOW IN HYDRATED RATS AND DOGS

1959 ◽  
Vol XXXII (I) ◽  
pp. 134-141 ◽  
Author(s):  
Niels A. Thorn
Keyword(s):  
Arginine Vasopressin ◽  
Urine Osmolality ◽  
Urine Flow ◽  
The Other ◽  
Maximum Increase ◽  
Urinary Osmolality ◽  
Lysine Vasopressin

ABSTRACT Arginine-, lysine- and leucine-vasopressin, injected i. v. into hydrated rats or dogs caused different patterns of response in that urine osmolality fell much more slowly after the maximum increase following arginine-vasopressin, than after the other two preparations. Using 3 different parameters for antidiuretic response, arginine-vasopressin was somewhat more potent than leucine-vasopressin in both rats and dogs, considerably more potent than lysine-vasopressin in rats, and much more so in dogs.

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.

Volumetric control of arginine vasotocin and mesotocin release in the frog (Rana ridibunda)

1985 ◽  
Vol 105 (3) ◽  
pp. 371-377 ◽  
Author(s):  
E. J. Nouwen ◽  
E. R. Kühn
Keyword(s):  
Plasma Levels ◽  
Plasma Concentrations ◽  
Control Level ◽  
Urine Osmolality ◽  
Ringer Solution ◽  
Urine Flow ◽  
Arginine Vasotocin ◽  
Rana Ridibunda ◽  
And Control ◽  
Control Plasma

ABSTRACT Adult male frogs (Rana ridibunda) were subjected to several volumetric and osmometric stimuli and the influence on circulating concentrations of arginine vasotocin (AVT) and mesotocin was studied by the use of highly specific radioimmunoassays. During progressive blood withdrawal (haemorrhage group) urine flow decreased to zero, whereas no change occurred in the plasma and urine osmolality. Control levels of 34·3±7·3 pmol AVT/1 gradually increased up to 638·3±179·1 pmol/l (P<0·001) after a blood loss of up to 50–60% of the blood volume. Plasma mesotocin concentrations also increased from 42·4±9·2 to 70·8±12·0 pmol/l (n = 7). Hypervolaemia, produced by the repeated intravenous injection of isotonic Ringer solution, increased the urine flow and osmolality compared to controls but had no influence on the plasma levels of AVT and mesotocin. Hypernatraemia without volume change profoundly increased the urine osmolality but the urine flow was not affected; the plasma concentrations of AVT and mesotocin remained at the control level. Finally, during a 1-h immobilization stress a pronounced antidiuresis occurred in the presence of a constant plasma and urine osmolality and control plasma levels of AVT and mesotocin. It is concluded that the release of AVT and, to a smaller extent, of mesotocin is under volumetric control. J. Endocr. (1985) 105, 371–377

scholarly journals Partial nephrogenic diabetes insipidus associated with lithium therapy

2019 ◽  
Vol 12 (9) ◽  
pp. e231093 ◽  
Author(s):  
Eka Nandoshvili ◽  
Steve Hyer ◽  
Nikhil Johri
Keyword(s):  
Diabetes Insipidus ◽  
Affective Disorder ◽  
Water Intake ◽  
Intramuscular Injection ◽  
Nephrogenic Diabetes Insipidus ◽  
Water Deprivation ◽  
Bipolar Affective Disorder ◽  
Urine Osmolality ◽  
Urinary Concentrating Ability

A 40-year-old Caucasian man developed excessive thirst and polyuria particularly at night over the preceding 6 months. He had been taking lithium for 16 years for the treatment of bipolar affective disorder. Investigations revealed subnormal maximum urinary concentrating ability after 8 hours of water deprivation and only a borderline response of urine osmolality to exogenous desmopressin given by intramuscular injection. A plasma copeptin concentration was elevated at 23 pmol/L. These results were consistent with partial nephrogenic diabetes insipidus. He was encouraged to increase his water intake as dictated by his thirst. In addition, he received amiloride with some improvement in his symptoms. Clinicians should be aware of the risk of nephrogenic diabetes insipidus with long-term lithium use and seek confirmation by a supervised water deprivation test augmented with a baseline plasma copeptin. If increased water intake is insufficient to control symptoms, amiloride may be considered.

Mechanism of cold diuresis in the rat

1983 ◽  
Vol 244 (2) ◽  
pp. F210-F216 ◽  
Author(s):  
M. L. Morgan ◽  
R. J. Anderson ◽  
M. A. Ellis ◽  
T. Berl
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Hemodynamic Parameters ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
6 Hydroxydopamine ◽  
Renal Water Excretion

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.

COX-2 disruption leads to increased central vasopressin stores and impaired urine concentrating ability in mice

2011 ◽  
Vol 301 (6) ◽  
pp. F1303-F1313 ◽  
Author(s):  
Rikke Nørregaard ◽  
Kirsten Madsen ◽  
Pernille B. L. Hansen ◽  
Peter Bie ◽  
Sugarna Thavalingam ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Collecting Duct ◽  
Mrna Level ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Glomerular Injury ◽  
Plasma Urea ◽  
Cox 2 ◽  
Response To Water ◽  
Urine Concentrating Ability

It was hypothesized that cyclooxygenase-2 (COX-2) activity promotes urine concentrating ability through stimulation of vasopressin (AVP) release after water deprivation (WD). COX-2-deficient (COX-2−/−, C57BL/6) and wild-type (WT) mice were water deprived for 24 h, and water balance, central AVP mRNA and peptide level, AVP plasma concentration, and AVP-regulated renal transport protein abundances were measured. In male COX-2−/−, basal urine output and water intake were elevated while urine osmolality was decreased compared with WT. Water deprivation resulted in lower urine osmolality, higher plasma osmolality in COX-2−/− mice irrespective of gender. Hypothalamic AVP mRNA level increased and was unchanged between COX-2−/− and WT after WD. AVP peptide content was higher in COX-2−/− compared with WT. At baseline, plasma AVP concentration was elevated in conscious chronically catheterized COX-2−/− mice, but after WD plasma AVP was unchanged between COX-2−/− and WT mice (43 ± 11 vs. 70 ± 16 pg/ml). Renal V2 receptor abundance was downregulated in COX-2−/− mice. Medullary interstitial osmolality increased and did not differ between COX-2−/− and WT after WD. Aquaporin-2 (AQP2; cortex-outer medulla), AQP3 (all regions), and UT-A1 (inner medulla) protein abundances were elevated in COX-2−/− at baseline and further increased after WD. COX-2−/− mice had elevated plasma urea and creatinine and accumulation of small subcapsular glomeruli. In conclusion, hypothalamic COX-2 activity is not necessary for enhanced AVP expression and secretion in response to water deprivation. Renal medullary COX-2 activity negatively regulates AQP2 and -3. The urine concentrating defect in COX-2−/− is likely caused by developmental glomerular injury and not dysregulation of AVP or collecting duct aquaporins.

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.

Increased PGE2 excretion by dDAVP in humans depends on state of hydration

1986 ◽  
Vol 250 (6) ◽  
pp. F1008-F1012 ◽  
Author(s):  
U. Schwertschlag ◽  
J. G. Gerber ◽  
J. S. Barnes ◽  
A. S. Nies
Keyword(s):  
Water Deprivation ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Water Diuresis ◽  
Water Load ◽  
Water Ingestion ◽  
Transient Rise ◽  
Relationship Of ◽  
The Relationship

The relationship of renal prostaglandin E2 (PGE2) excretion (UPGEV) to water deprivation, water diuresis, and subsequent antidiuresis by 1-desamino-8-D-arginine vasopressin (dDAVP) was studied in female volunteers. After 16 h of water deprivation, the subjects began a sustained water diuresis for 8 h. This diuresis caused a transient twofold rise in UPGEV at 2 h (P less than 0.05), which then fell back to or below baseline levels. dDAVP given during the water diuresis caused a transient rise of UPGEV as urine volume decreased and plasma osmolality fell from 277 +/- 1.5 to 271 +/- 2 mosmol/kg (P less than 0.01). Another group of subjects had the water diuresis discontinued after 4 h with dDAVP given at the 5th h when urine volume was decreasing and urine osmolality was increasing. In this setting dDAVP did not produce as great a fall in plasma osmolality nor did it increase UPGEV. These data indicate that renal prostaglandin synthesis (as determined by UPGEV) is increased transiently by an acute water load; dDAVP given during continued water ingestion results in a fall in plasma osmolality and increased PGE excretion; however, dDAVP does not increase UPGEV during normal hydration; and UPGEV is independent of changes in urine flow. These findings imply that renal prostaglandins may have a functional role in humans to inhibit the hydroosmotic actions of antidiuretic hormone, and thus hasten the excretion of a water load, and to prevent overhydration when inappropriate antidiuresis occurs. However, there is no evidence that the stimulus for prostaglandin production is dDAVP per se.

EVIDENCE THAT THE ANTIDIURETIC SUBSTANCE IN THE PLASMA OF CHILDREN WITH NEPHROGENIC DIABETES INSIPIDUS IS ANTIDIURETIC HORMONE

PEDIATRICS ◽  
1963 ◽  
Vol 32 (3) ◽  
pp. 384-388
Author(s):  
Malcolm A. Holliday ◽  
Charles Burstin ◽  
Jean Harrah
Keyword(s):  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Nephrogenic Diabetes Insipidus ◽  
Water Deprivation ◽  
Jugular Vein ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Antidiuretic Activity ◽  
Antecubital Vein ◽  
Assay Technique

The antidiuretic activity in the plasma of four children with nephrogenic diabetes insipidus was measured by a rat assay technique. The evidence presented to indicate that this activity was due to antidiuretic hormone (ADH) was as follows: (a) the activity was higher in jugular vein plasma than in femoral or antecubital vein plasma, (b) it was high when the children were thirsted and decreased when they drank water, (c) it was destroyed when the plasma was incubated with thioglycollate, and (d) it was ultrafilterable, and vasopressin (Pitressin), when injected, was distributed as though it was ultrafilterable. When the children were given vasopressin, there was no change in urine flow or osmolality, but plasma antidiuretic activity was higher than it was when water deprivation led to a reduction in urine flow and an increase in urine osmolality. The inference of these findings is that ADH is secreted normally in children with nephrogenic diabetes insipidus, it is ultrafilterable, but it is not a factor in modifying urine flow in response to dehydration.

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