Impairment of osmotically stimulated AVP release in patients with primary polydipsia

1993 ◽  
Vol 265 (6) ◽  
pp. R1247-R1252 ◽  
Author(s):  
A. M. Moses ◽  
B. Clayton

The secretion of arginine vasopressin (AVP) from the posterior pituitary is primarily and finely regulated by the osmolality of plasma. Even though a number of factors alter osmolality-induced release of AVP, there are no published data in humans that have addressed the role of chronic overhydration on this phenomenon. To address this problem we have identified eight patients with primary polydipsia using criteria not involving measurement of AVP, and have subjected them to standardized infusions of hypertonic saline. These patients had less AVP in both plasma and urine in relation to plasma osmolality than was found in normal subjects. In addition, their rate of rise of plasma and urine AVP was less than in normal subjects. Their osmotic threshold for AVP release may have been higher than normal. These data demonstrate that chronic overhydration in humans downregulates the release of AVP in response to hypertonicity. This phenomenon may explain the impairment of urine concentration in patients with primary polydipsia and emphasizes the basis of the difficulty that may occur clinically in differentiating between patients with primary polydipsia and partial central diabetes insipidus.

1992 ◽  
Vol 127 (6) ◽  
pp. 494-498 ◽  
Author(s):  
MA Arnaout ◽  
K Ajlouni

The neurohypophyseal function was assessed in a group of 15 patients with postpartum hypopituitarism by measuring plasma arginine-vasopressin concentrations during 5% hypertonic saline infusion. None of the patients had symptoms of diabetes insipidus and all patients were on adequate cortisone and thyroxine replacement therapy before testing. The mean basal plasma vasopressin value in the patients (0.6±0.1 pmol/1) was significantly lower than that in the normal subjects (2.9±0.3 pmol/l; p<0.01), whereas the mean serum sodium, plasma osmolality, plasma renin activity and serum aldosterone values were similar in the two groups. During the osmolar load (5% hypertonic saline), the patients revealed varying degrees of arginine-vasopressin responses to the increase in plasma osmolality. Three patients showed normal arginine-vasopressin responses, 10 had subnormal responses, and 2 had no response. During the dehydration test, the patients revealed significantly lower maximum urine osmolalities (p<0.0025) with significantly higher concurrent mean plasma osmolality (p<0.0025) than the controls. None of the patients showed overt polyuria at the time of the study. The results indicate the impaired osmoregulation of arginine-vasopressin secretion to an osmolar stimuli in patients with postpartum hypopituitarism, suggesting neurohypophyseal damage. In patients with Sheehan's syndrome, partial diabetes insipidus seems to be much more frequent than previously believed.


2015 ◽  
Vol 4 (2) ◽  
pp. 86-91 ◽  
Author(s):  
M de Fost ◽  
S M Oussaada ◽  
E Endert ◽  
G E Linthorst ◽  
M J Serlie ◽  
...  

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.


2010 ◽  
pp. 1819-1825
Author(s):  
Aparna Pal ◽  
Niki Karavitaki ◽  
John A. H. Wass

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....


1994 ◽  
Vol 267 (2) ◽  
pp. H751-H756 ◽  
Author(s):  
A. W. Cowley ◽  
E. Szczepanska-Sadowska ◽  
K. Stepniakowski ◽  
D. Mattson

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.


1992 ◽  
Vol 126 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Tokihisa Kimura ◽  
Kozo Ota ◽  
Masaru Shoji ◽  
Minoru Inoue ◽  
Kazutoshi Sato ◽  
...  

To assess whether arginine vasopressin and atrial natriuretic hormone participate in impaired urinary dilution and excretion in glucocorticoid deficiency secondary to hypopituitarism. an acute oral water load of 20 ml·kg−1 BW was undertaken in the absence and presence of an oral hydrocortisone (60 mg) treatment in patients with ACTH deficiency (N= 7) and panhypopituitarism (N = 2). Plasma arginine vasopressin and atrial natriuretic hormone and renal water handling were simultaneously determined and compared with those in similarly water-loaded normal subjects. Plasma arginine vasopressin did not fall in response to decreased blood osmolality after an acute water load in the absence of hydrocortisone; plasma atrial natriuretic hormone did not change despite blood volume expansion; and impairment in urinary dilution and excretion remained. On the other hand, in the presence of hydrocortisone, plasma arginine vasopressin fell in response to a decrease in plasma osmolality and plasma atrial natriuretic hormone increased, thereby restoring urinary dilution and excretion. These results demonstrate that the impaired arginine vasopressin response to acute water loading play an essential role in deranged renal water and electrolyte handling in the state of glucocorticoid deficiency; the impaired release of atrial natriuretic hormone also may affect these disorders.


1983 ◽  
Vol 29 (5) ◽  
pp. 882-884 ◽  
Author(s):  
J Camps ◽  
A Martínez-Vea ◽  
R M Pérez-Ayuso ◽  
V Arroyo ◽  
J M Gaya ◽  
...  

Abstract A radioimmunoassay for arginine-vasopressin in human plasma with use of a commercially available antibody was developed and evaluated. The hormone was extracted from plasma with cold 98% ethanol, which showed a significantly higher (p less than .001) and more precise recovery than with the acetone-ether procedure (65.3 +/- 3.7% vs 50.8 +/- 6.0%, respectively). The sensitivity was 0.31 pg per tube. Results for normal subjects in different physiological conditions and in patients with diabetes insipidus and inappropriate antidiuretic hormone secretion showed the good reliability of the method.


2007 ◽  
Vol 292 (2) ◽  
pp. F868-F875 ◽  
Author(s):  
Chris R. J. Kennedy ◽  
Huaqi Xiong ◽  
Sherine Rahal ◽  
Jacqueline Vanderluit ◽  
Ruth S. Slack ◽  
...  

We investigated the role of the prostaglandin E2 (PGE2) EP1 receptor in modulating urine concentration as it is expressed along the renal collecting duct where arginine-vasopressin (AVP) exerts its anti-diuretic activity, and in the paraventricular and supraoptic nuclei of the hypothalamus where AVP is synthesized. The urine osmolality of EP1-null mice (EP1−/−) failed to match levels achieved by wild-type (WT) counterparts upon water deprivation (WD) for 24 h. This difference was reflected by higher plasma osmolality in WD EP1−/− mice. Along the collecting duct, the induction and subapical to plasma membrane translocation of the aquaporin-2 water channel in WD EP1−/− mice appeared equivalent to that of WD WT mice as determined by quantitative RT-PCR and immunohistochemistry. However, medullary interstitial osmolalities dropped significantly in EP1−/− mice following WD. Furthermore, urinary AVP levels of WD EP1−/− mice were significantly lower than those of WD WT mice. This deficit could be traced back to a blunted induction of hypothalamic AVP mRNA expression in WD EP1−/− mice as determined by quantitative RT-PCR. Administration of the AVP mimetic [deamino-Cys1,d-Arg8]-vasopressin restored a significant proportion of the urine concentrating ability of WD EP1−/− mice. When mice were water loaded to suppress endogenous AVP production, urine osmolalities increased equally for WT and EP1−/− mice. These data suggest that PGE2 modulates urine concentration by acting at EP1 receptors, not in the collecting duct, but within the hypothalamus to promote AVP synthesis in response to acute WD.


1981 ◽  
Vol 240 (3) ◽  
pp. R182-R186
Author(s):  
R. M. Jones ◽  
F. T. LaRochelle ◽  
S. M. Tenney

Normal rats (N) and rats with hereditary hypothalamic diabetes insipidus (DI) were employed to examine the role of arginine vasopressin (AVP) in the reduction of water intake and urine output during hypoxic exposure. The pattern of reduced water intake followed by recovery was similar in both N and DI rats during 7 days of hypobaric hypoxia (inspired O2 pressure of 75 Torr). Water intake was markedly reduced during the first 6 h of hypoxic exposure in both groups, whereas urine output did not decrease significantly until after 6 h in DI rats and after 18 h in N rats. Total urinary excretion of AVP in N rats decreased and remained depressed during 7 days of hypoxia. (AVP excretion corrected for osmolar clearance was unchanged.) Plasma AVP of conscious N rats was 2.7 +/- 0.40 pg/ml plasma during normoxia and 2.4 +/- 0.74 pg/ml plasma after 2 h of exposure to inspired O2 fractional concentrations of 0.105 (paired samples). We conclude that AVP is not a major factor in the decreased water intake and urine output observed during hypoxia, and that the initial disturbance is a reduced water intake that leads to negative water balance, reduced urine volume, increased urine concentration, and hyperosmotic volume contraction. The reduced or unchanged AVP release in normal rats during hypoxia appears to be inappropriate.


1988 ◽  
Vol 117 (1) ◽  
pp. 13-18 ◽  
Author(s):  
D. B. Dunger ◽  
J. R. Seckl ◽  
D. B. Grant ◽  
L. Yeoman ◽  
S. L. Lightman

Abstract. The value of a 7-h water deprivation test incorporating urinary osmolality and urinary arginine vasopressin (AVP) measurements was investigated in 20 children with suspected anterior or posterior pituitary dysfunction (group A) and 11 presenting with polyuria and polydipsia (group B). A control group of 16 healthy children was also studied. Urinary osmolalities in the control subjects after 7 h of water deprivation were 827–1136 mosmol/kg and urinary AVP 114–320 pmol/l. Of the group A patients, 5 had symptomatic diabetes insipidus with urinary osmolalities < 300 mosmol/kg, and urinary AVP concentrations of < 10 pmol/l, and 5 had normal urinary concentrating ability. The other 10 patients had varying degrees of partial diabetes insipidus (urinary AVP 6–53 pmol/l) although in 3 urinary concentrating ability was well maintained (osmolality 650–747 mosmol/kg). In group B, a diagnosis of compulsive water drinking was made in 9 patients, 1 had nephrogenic diabetes insipidus (urinary osmolality 68 mosmol/kg, AVP 782 pmol/l), and the final patient had transient diabetes insipidus. The test described was easy to perform and well tolerated even in young children. Using this test alone, it was possible to identify patients with partial defects of posterior pituitary function even when urinary concentrating ability was maintained, as well as those with complete cranial diabetes insipidus, nephrogenic diabetes insipidus, and compulsive water drinking.


1997 ◽  
pp. 162-166 ◽  
Author(s):  
M Knoepfelmacher ◽  
MJ Pradal ◽  
RD Dio ◽  
LR Salgado ◽  
M Semer ◽  
...  

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.


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