Effect of Carbamazepine on Plasma and Urine Arginine-Vasopressin

1978 ◽  
Vol 54 (4) ◽  
pp. 419-424 ◽  
Author(s):  
T. H. Thomas ◽  
S. G. Ball ◽  
J. K. Wales ◽  
M. R. Lee
Keyword(s):  
Drug Treatment ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Direct Action ◽  
Control Period ◽  
Urine Osmolality ◽  
Normal Subjects ◽  
Plasma Sodium ◽  
Sodium Plasma

1. Five normal subjects were studied before and during treatment with carbamazepine. 2. Plasma sodium, plasma and urine arginine-vasopressin and urine osmolality were measured during a day of water deprivation, before and during drug treatment. 3. During treatment with carbamazepine plasma sodium increased whereas plasma and urine arginine-vasopressin and urine osmolality decreased. Plasma and urine arginine-vasopressin were significantly correlated with urine osmolality. However, carbamazepine did not affect the osmolality of urine produced by the kidney, in response to endogenous arginine-vasopressin. 4. Plasma and urine arginine-vasopressin were significantly correlated with plasma sodium on both control and drug-treatment days, but the relationships of plasma and urine arginine-vasopressin to plasma sodium were different during carbamazepine treatment, as compared with the control period. 5. It is suggested that the threshold of the hypothalamic osmoreceptors for release of arginine-vasopressin is modified by carbamazepine, and that this may be either a direct action or secondary to another action of the drug.

scholarly journals Apelin Counteracts Vasopressin-Induced Water Reabsorption via Cross Talk Between Apelin and Vasopressin Receptor Signaling Pathways in the Rat Collecting Duct

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4483-4493 ◽  
Author(s):  
Annette Hus-Citharel ◽  
Laurence Bodineau ◽  
Alain Frugière ◽  
Fanny Joubert ◽  
Nadine Bouby ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Cross Talk ◽  
Arginine Vasopressin ◽  
Blood Circulation ◽  
Direct Action ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Water Reabsorption ◽  
Collecting Ducts ◽  
Antagonist Effect

Abstract Apelin receptors (ApelinRs) are expressed along an increasing cortico-medullary gradient in collecting ducts (CDs). We showed here that iv injection of apelin 17 (K17F) in lactating rats characterized by increases in both synthesis and release of arginine vasopressin (AVP) increased diuresis concomitantly with a significant decrease in urine osmolality and no change in Na+ and K+ excretion. Under these conditions, we also observed a significant decrease in apical aquaporin-2 immunolabeling in CD, with a cortico-medullary gradient, suggesting that K17F-induced diuresis could be linked to a direct action of apelin on CD. We then examined the potential cross talk between V1a AVP receptor (V1a-R), V2 AVP receptor (V2-R) and ApelinR signaling pathways in outer medullary CD (OMCD) and inner medullary CD microdissected rat CD. In OMCD, expressing the 3 receptors, K17F inhibited cAMP production and Ca2+ influx induced by 1-desamino-8-D-arginine vasopressin a V2-R agonist. Similar effects were observed in inner medullary CD expressing only V2-R and ApelinR. In contrast, in OMCD, K17F increased by 51% the Ca2+ influx induced by the stimulation of V1a-R by AVP in the presence of the V2-R antagonist SR121463B, possibly enhancing the physiological antagonist effect of V1a-R on V2-R. Thus, the diuretic effect of apelin is not only due to a central effect by inhibiting AVP release in the blood circulation as previously shown but also to a direct action of apelin on CD, by counteracting the antidiuretic effect of AVP occurring via V2-R.

scholarly journals Collecting duct-specific knockout of adenylyl cyclase type VI causes a urinary concentration defect in mice

2012 ◽  
Vol 302 (1) ◽  
pp. F78-F84 ◽  
Author(s):  
Karl P. Roos ◽  
Kevin A. Strait ◽  
Kalani L. Raphael ◽  
Mitsi A. Blount ◽  
Donald E. Kohan
Keyword(s):  
Adenylyl Cyclase ◽  
Water Intake ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Collecting Duct ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Camp Accumulation ◽  
Water Excretion ◽  
Normal Water

Collecting duct (CD) adenylyl cyclase VI (AC6) has been implicated in arginine vasopressin (AVP)-stimulated renal water reabsorption. To evaluate the role of CD-derived AC6 in regulating water homeostasis, mice were generated with CD-specific knockout (KO) of AC6 using the Cre/loxP system. CD AC6 KO and controls were studied under normal water intake, chronically water loaded, or water deprived; all of these conditions were repeated in the presence of continuous administration of 1-desamino-8-d-arginine vasopressin (DDAVP). During normal water intake or after water deprivation, urine osmolality (Uosm) was reduced in CD AC6 KO animals vs. controls. Similarly, Uosm was decreased in CD AC6 KO mice vs. controls after water deprivation+DDAVP administration. Pair-fed (with controls) CD AC6 KO mice also had lower urine osmolality vs. controls. There were no detectable differences between KO and control animals in fluid intake or urine volume under any conditions. CD AC6 KO mice did not have altered plasma AVP levels vs. controls. AVP-stimulated cAMP accumulation was reduced in acutely isolated inner medullary CD (IMCD) from CD A6 KO vs. controls. Medullary aquaporin-2 (AQP2) protein expression was lower in CD AC6 KO mice vs. controls. There were no differences in urinary urea excretion or IMCD UT-A1 expression; however, IMCD UT-A3 expression was reduced in CD AC6 KO mice vs. controls. In summary, AC6 in the CD regulates renal water excretion, most likely through control of AVP-stimulated cAMP accumulation and AQP2.

Resistance to vasopressin action on the kidney in patients with Cushing's disease

1997 ◽  
pp. 162-166 ◽  
Author(s):  
M Knoepfelmacher ◽  
MJ Pradal ◽  
RD Dio ◽  
LR Salgado ◽  
M Semer ◽  
...  
Keyword(s):  
Normal Control ◽  
Arginine Vasopressin ◽  
Cushing’S Disease ◽  
Plasma Levels ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Normal Subjects ◽  
Cushing's Disease ◽  
Urinary Osmolality ◽  
Normal Individuals

OBJECTIVE: To assess the plasma levels and action of arginine vasopressin (AVP) in patients with Cushing's disease. There are many reports that patients with Addison's disease have increased AVP levels associated with hyponatraemia and hypoosmolality, but none on the dynamics of secretion of this neurohormone during osmolality-based stimulation in patients with chronic hypercortisolism. DESIGN AND SUBJECTS: The plasma AVP concentration and the urinary and plasma osmolality after a 7.5-h water deprivation test (WDT) were evaluated in 13 patients with Cushing's disease and 15 normal (control) individuals. In patients with Cushing's disease we also assessed the urinary osmolality in response to 10 micrograms i.v. desmopressin (DDAVP) administered at the end of the WDT. RESULTS: At the end of the WDT, urinary osmolality was significantly lower in patients with Cushing's disease (511.5 +/- 148.5 mOsm/l) than in the normal subjects (981.1 +/- 107.1 mOsm/l, P < 0.001), whereas plasma osmolality did not differ between the two groups. Consequently, the urine/plasma osmolality ratio (Uosm/Posm) was lower in patients with Cushing's disease than in normal individuals (1.8 +/- 0.5 compared with 3.4 +/- 0.4, P < 0.001). The AVP concentration also was greater (7.3 +/- 3.1 pmol/l) in those with Cushing's disease than in the controls (3.9 +/- 2.3 pmol/l, P < 0.005). After administration of DDAVP to the hypercortisolaemic patients, the urinary osmolality attained (718.0 +/- 200.0 mOsm/l) was still lower than that in the normal group at the end of WDT (P < 0.005). CONCLUSIONS: Patients with Cushing's disease presented higher AVP levels and smaller Uosm/Posm ratios than normal subjects. After DDAVP, the patients with Cushing's disease were unable to concentrate the urine adequately. These data suggest that the kidney shows resistance to the action of both endogenous and exogenous AVP in patients with Cushing's disease.

Effects of drinking on thirst and vasopressin in dehydrated elderly men

1993 ◽  
Vol 264 (5) ◽  
pp. R877-R881 ◽  
Author(s):  
P. A. Phillips ◽  
M. Bretherton ◽  
J. Risvanis ◽  
D. Casley ◽  
C. Johnston ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
The Elderly ◽  
Young Group ◽  
Plasma Sodium ◽  
Elderly Men ◽  
Water Load ◽  
Water Deficits ◽  
Healthy Elderly

Inhibition of dehydration-induced arginine vasopressin (AVP) secretion and thirst depends on removal of osmotic and hemodynamic stimuli as well as on preabsorptive oropharyngeal factors that reduce thirst and AVP secretion on drinking before correction of the water deficits. Plasma atrial natriuretic peptide (ANP) levels may also change with drinking. Therefore, the thirst and plasma responses to oral water loads (10 ml/kg) in 10 healthy old (64-76 yr) and young (20-32 yr) 24-h water-deprived men were investigated. After 24-h water deprivation plasma sodium, osmolality, and AVP were increased similarly in both groups (P < 0.001). Plasma ANP levels fell after dehydration similarly in both groups (P < 0.05) but were always higher in the older group (P < 0.05). However, although thirst increased in both groups (P < 0.05), this was significantly less in the elderly (P < 0.05). After the water load, thirst was reduced in both groups throughout the study (P < 0.05). However, plasma AVP fell immediately after drinking only in the young group and rose to postdeprivation levels after 15 min. Plasma AVP was not different from postdeprivation throughout in the old group and after 15 min in the young group presumably because the water load was insufficient to replace their water deficits. In the young group only, plasma ANP rose to 182 +/- 43% of postdeprivation levels at 3 min after drinking (P < 0.05). These results demonstrate reduced oropharyngeal inhibition of AVP secretion after drinking in healthy elderly men but maintained inhibition of thirst.

Water conservation following prolonged vasopressin administration

1960 ◽  
Vol 198 (5) ◽  
pp. 1129-1133 ◽  
Author(s):  
Walter Hollander ◽  
William B. Blythe
Keyword(s):  
Water Conservation ◽  
Water Deprivation ◽  
Direct Action ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Serum Osmolality ◽  
Prolonged Administration ◽  
Water Imbibition ◽  
Significant Difference ◽  
And Control

Rats were injected with vasopressin tannate in oil twice daily for 80 days and aqueous vasopressin every 4 hours for the next 3 days. During vasopressin administration, spontaneous water imbibition was less than and serum osmolality remained the same as that of controls receiving peanut oil. After 80 days, renal response to vasopressin was still normal. Beginning 4 hours after vasopressin was stopped, rats were subjected to a 3-day period of water deprivation during which there was no significant difference between previously vasopressin-treated and control rats with respect to: a) urine volume and urine osmolality measured at 12-hour intervals; b) weight loss; c) rise in serum osmolality. No polydipsia developed during 4 weeks after vasopressin was discontinued. It is concluded that prolonged administration of vasopressin to rats does not cause even transient subsequent impairment of water conservation mechanisms including neurohypophyseal release of ADH. This may imply that regulation of ADH secretion does not include a ‘feed-back’ mechanism involving a direct action of circulating ADH on the hypothalamic-neurohypophyseal system.

Inter-relationship between urinary kallikrein-kinins and arginine vasopressin in man

1989 ◽  
Vol 76 (1) ◽  
pp. 13-18 ◽  
Author(s):  
K. Yamada ◽  
K. Hasunuma ◽  
T. Shiina ◽  
K. Ito ◽  
Y. Tamura ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Arginine Vasopressin ◽  
Control Period ◽  
Urine Volume ◽  
Free Water ◽  
Normal Subjects ◽  
Urine Flow ◽  
Urinary Kallikrein ◽  
Plasma Aldosterone Concentration ◽  
Water Loading

1. Physiological saline solution was infused in nine normal subjects and six patients with central diabetes insipidus (DI). At 120 min after the start of infusion, arginine vasopressin (AVP) was injected intramuscularly. Urine was collected in 30 min fractions before and after AVP administration. 2. The urinary excretions of kallikrein-like activity (KAL-A) (S-2266 hydrolysis activity) and immunoreactive kinins (i-kinins) were significantly lower in patients with DI than in normal subjects before AVP administration, while there were no differences in plasma renin activity, plasma aldosterone concentration, creatinine clearance and blood pressure between the two groups, except for a marked water diuresis in patients with DI. The urinary excretion of KAL-A and i-kinins correlated positively with the urinary excretion of AVP. 3. AVP administration increased both plasma AVP and urinary excretion of AVP to similar levels in both groups. As a result, urine volume decreased to a greater degree in patients with DI than in normal subjects. In contrast, the urinary excretions of KAL-A and i-kinins were increased by AVP administration, with a greater response in normal subjects than in the patients with DI. 4. After overnight fasting, acute water loading was carried out orally for 15 min in six normal subjects. At 30 min plasma AVP was suppressed by water loading to almost the basal level found in patients with DI. Urinary excretions of KAL-A and i-kinins in the first 30 min fraction after loading were also suppressed to the basal level in patients with DI. Later, the urinary excretion of KAL-A increased together with the increase in urine flow. Urine volume and free water clearance markedly increased except in the first 30 min fraction, compared with the control period. 5. Thus it is suggested that AVP is one of the factors regulating the renal kallikrein-kinin system in man, although it seems likely that urine flow is still a major factor in urinary kallikrein-kinin excretion.

scholarly journals The water deprivation test and a potential role for the arginine vasopressin precursor copeptin to differentiate diabetes insipidus from primary polydipsia

2015 ◽  
Vol 4 (2) ◽  
pp. 86-91 ◽  
Author(s):  
M de Fost ◽  
S M Oussaada ◽  
E Endert ◽  
G E Linthorst ◽  
M J Serlie ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Arginine Vasopressin ◽  
Clinical Judgment ◽  
Gold Standard ◽  
Diagnostic Performance ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Water Deprivation Test ◽  
Primary Polydipsia

The water deprivation test is the gold standard test to differentiate central or nephrogenic diabetes insipidus (DI) from primary polydipsia (PP) in patients with polyuria and polydipsia. Few studies have addressed the diagnostic performance of this test. The aim of this retrospective cohort study was to evaluate the diagnostic performance of the standard water deprivation test, including plasma arginine vasopressin (AVP) measurements, in 40 consecutive patients with polyuria. We compared initial test results with the final clinical diagnosis, i.e., no DI, central DI, or nephrogenic DI. The median length of follow-up was 8 years. In a subset of ten patients, the novel marker copeptin (CP) was measured in plasma. Using the final diagnosis as a gold standard, a threshold for urine osmolality of >800 mOsmol/kg after water deprivation yielded a sensitivity and specificity of 96 and 100%, respectively, for diagnosing PP. Sensitivity increased to 100% if the cut-off value for urine osmolality was set at 680 mOsmol/kg. Plasma AVP levels did not differ between patient groups and did not differentiate among central DI, nephrogenic DI, or PP. In all three patients with central DI, plasma CP was <2.5 pmol/l with plasma osmolality >290 mOsmol/kg, and >2.5 pmol/l in patients without DI. The optimal cut-off value for differentiating PP from DI during a water deprivation test was urine osmolality >680 mOsmol/kg. Differentiating between central and nephrogenic DI should be based on clinical judgment as AVP levels did not discriminate.

Disorders of the posterior pituitary gland

2010 ◽  
pp. 1819-1825
Author(s):  
Aparna Pal ◽  
Niki Karavitaki ◽  
John A. H. Wass
Keyword(s):  
Pituitary Gland ◽  
Diabetes Insipidus ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Posterior Pituitary ◽  
Posterior Pituitary Gland ◽  
Long Acting ◽  
Cranial Diabetes Insipidus

The posterior pituitary produces arginine vasopressin, which has a key role in fluid homeostasis, and oxytocin, which stimulates uterine contraction during birth and ejection of milk during lactation. Cranial diabetes insipidus is the passage of large volumes (>3 litres/24 h) of dilute urine (osmolality<300 mOsm/kg) due to vasopressin deficiency, and most commonly occurs as a consequence of trauma or tumour affecting the posterior pituitary. Diagnosed by a water deprivation test revealing urine osmolality less than 300 mOsml/kg with concurrent plasma osmolality more than 290 mOsml/kg after dehydration, with urine osmolality rising to more than 750 mOsml/kg after desmopressin. MRI of the neurohypophysis is required to delineate the cause. Mild polyuria can be managed simply by ensuring adequate fluid intake; treatment with the long-acting vasopressin analogue, desmopressin (desamino, D-8 arginine vasopressin; DDAVP), is used for more severe cases....

Mechanism of drinking-induced inhibition of vasopressin secretion in dehydrated dogs

1991 ◽  
Vol 261 (5) ◽  
pp. R1226-R1233 ◽  
Author(s):  
B. H. Appelgren ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Control Experiment ◽  
Control Period ◽  
Easy Access ◽  
Inhibitory Input ◽  
Inhibitory Mechanism ◽  
Blood Samples ◽  
Time Control ◽  
Vasopressin Secretion

Ingestion of water stimulates a powerful inhibitory input to secretion of arginine vasopressin (AVP) in many species. A previous study in dogs has suggested that the stimulus arises from activation of oropharyngeal receptors, but the nature of the stimulus is unknown. The objectives of this study were to determine if the taste, osmolality, or temperature of the solution ingested constituted an important element in the inhibitory mechanism and if these same attributes affected the volume ingested in response to 24 h of water deprivation in conscious dogs. Experiments consisted of a control period, a 6-min period of access to fluid, and a 60-min period after drinking, with blood samples taken frequently to assess changes in plasma AVP. Dogs were placed in a sling that allowed them to stand or lie supported with easy access to a bowl. The solutions were water at 20 and 38 degrees C; 0.9% NaCl at 20 and 38 degrees C; 1.8 and 2.7% NaCl at 20 degrees C; 5% glucose and mannitol and 10% mannitol at 20 degrees C; and liquified food at 20 degrees C. In the time-control experiment dogs were allowed to see but not drink water for 6 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of water deprivation on urinary excretion of PGE2 in the dog

1983 ◽  
Vol 245 (3) ◽  
pp. R329-R333 ◽  
Author(s):  
A. Zucker ◽  
A. Nasjletti ◽  
E. G. Schneider
Keyword(s):  
Body Weight ◽  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Free Access ◽  
Access To Water

We examined the influence of the state of hydration on the urinary excretion of prostaglandin E2 (PGE2) and kallikrein in the dog. Immunoreactive PGE2 and kallikrein were measured in the urine of conscious dogs during periods of water deprivation and periods of free access to drinking water and in the urine of time-control dogs that had free access to water throughout the study. During water deprivation the excretion of kallikrein did not change significantly, but PGE2 excretion increased by 50 and 75% (P less than 0.05) after 2 and 4 days, respectively, associated with reductions of body weight and urine flow and with elevation of plasma renin activity, plasma sodium, and both plasma and urine osmolality. Dehydrated dogs drank copiously when allowed free access to water, and over the following 4 days both PGE2 excretion and plasma renin activity fell significantly, associated with elevation of body weight and urine volume and with lowering of plasma sodium and plasma and urine osmolality. In contrast, if after 4 days of water deprivation the dogs were kept at a constant level of dehydration by restricting their water allotment on subsequent days to 300 ml/day, PGE2 excretion and most other variables remained at the dehydration level. In conclusion, these results suggest that renal PGE2 production is dependent on the state of hydration in the dog.

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