Inappropriate vasopressin secretion in two dogs

1988 ◽  
Vol 117 (1) ◽  
pp. 59-64 ◽  
Author(s):  
A. Rijnberk ◽  
W. J. Biewenga ◽  
J. A. Mol

Abstract. Two dogs with hyponatremia due to inappropriate arginine vasopressin (AVP) secretion are described. Threshold and sensitivity of AVP secretion were investigated by increasing plasma osmolality with hypertonic saline infusion. In one dog, osmoregulation of AVP secretion occurred at normal sensitivity but at a low threshold. The other dog had a relatively high plasma AVP concentration under (resting) hypotonic conditions with an otherwise normal response to increasing plasma tonicity. In the absence of evidence for associated disease, it is suggested that both dogs have an idiopathic form of the syndrome of inappropriate AVP secretion.

1985 ◽  
Vol 110 (3) ◽  
pp. 346-351 ◽  
Author(s):  
Simon Smitz ◽  
Jean-Jacques Legros

Abstract. A patient with the chronic hypernatraemia syndrome is described. Using a sensitive and specific radioimmunoassay, the plasma arginine-vasopressin (AVP) level was measured under various conditions. With an unrestricted diet, the plasma AVP level was inappropriately low for the degree of plasma hyperosmolality (0.9 pmol/l and 302 mOsm/kg, respectively). After chronic water loading, plasma osmolality was 271 mOsm/kg, plasma AVP level 1.5 pmol/l, and the urine remained hypertonic with respect to the plasma. During hypertonic saline infusion, plasma osmolality increased from 271 to 294 mOsm/kg without a concomitant increase in the plasma AVP concentration. After sc injection of apomorphine and after haemodynamic stimulation, the plasma AVP concentration increased from 0.8 to 36 pmol/l and from 1.2 to 6.3 pmol/I, respectively. These data demonstrate a selective deficiency in the osmoregulation of the AVP secretion. The observed neuroendocrine abnormalities may be linked to a congenital malformation of the brain.


1991 ◽  
Vol 260 (3) ◽  
pp. R533-R539 ◽  
Author(s):  
C. J. Thompson ◽  
P. Selby ◽  
P. H. Baylis

We have studied the reproducibility of the thirst and arginine vasopressin (AVP) responses to osmotic and hypoglycemic stimulation in healthy volunteers undergoing repeat hypertonic (855 mmol/l) saline infusion and insulin tolerance tests (ITTs). Hypertonic saline infusion caused similar mean rises in plasma osmolality, AVP, and thirst on each occasion. Linear-regression analysis defined close relationships between the slopes (r = +0.72, P less than 0.05) and the abscissal intercepts (r = +0.89, P less than 0.001) of the regression lines relating plasma osmolality (Posmol) and plasma AVP (PAVP), and the group intraindividual component of the variance for the slopes and intercepts was 7 and 0.6%, respectively. There were close correlations between the slopes (r = +0.79, P less than 0.02) and the intercepts (r = +0.84, P less than 0.01) of the regression lines relating Posmol and thirst, and group intraindividual component of the variance was 14 and 0.7%, respectively. Hypertonic saline infusion was infused on four occasions in four subjects, and the results showed that the linear regression lines relating PAVP and Posmol and thirst and Posmol were reproducible within an individual. There were similar falls in blood glucose and elevations in PAVP in both ITTs. No relationship was defined between the fall in blood glucose and either the rise in PAVP or the area under the AVP curve (AUC). The intraindividual component of the variance for the rise in AVP and the AUC was 77 and 22.5%, respectively. The AVP and thirst responses to osmotic stimulation are highly reproducible, but there is considerable intraindividual variation in the AVP response to hypoglycemia.


1987 ◽  
Vol 252 (6) ◽  
pp. R1138-R1142 ◽  
Author(s):  
C. J. Thompson ◽  
J. M. Burd ◽  
P. H. Baylis

Drinking rapidly abolishes thirst and vasopressin secretion in dehydrated humans before major changes in plasma osmolality are observed. We studied the effects of drinking on plasma vasopressin and thirst in seven healthy volunteers rendered hypernatremic by the infusion of hypertonic (855 mmol/l) sodium chloride solution. Thirst was measured on a visual analogue scale (0-10 cm). Infusion of hypertonic saline caused linear increases in plasma osmolality (289 +/- 1 to 306 +/- 1 mosmol/kg, mean +/- SE, P less than 0.001), plasma vasopressin (0.6 +/- 0.2 to 6.4 +/- 1.9 pmol/l, P less than 0.001), and thirst (1.4 +/- 0.4 to 7.4 +/- 0.5 cm, P less than 0.001). Water was allowed 15 min after cessation of the infusion, and within 5 min of drinking both plasma vasopressin and thirst were significantly lower than postinfusion. After 20 min of drinking, plasma vasopressin had fallen from 6.5 +/- 0.9 to 1.3 +/- 0.3 pmol/l (P less than 0.001) and thirst from 7.7 +/- 0.5 to 1.0 +/- 0.2 cm (P less than 0.001) despite no significant change in plasma osmolality (306 +/- 0.9 to 304 +/- 0.8 mosmol/kg, P = 0.17), and the drinking of 1,200 +/- 60 ml of water, over 85% of the mean cumulative water intake in the 30-min drinking period. Control studies in the same subjects showed comparable rises in plasma vasopressin, plasma osmolality, and thirst during hypertonic saline infusion but no fall in any of these parameters during an equivalent 30-min period after the infusions, during which water was withheld.(ABSTRACT TRUNCATED AT 250 WORDS)


1994 ◽  
Vol 266 (2) ◽  
pp. H822-H828 ◽  
Author(s):  
M. Goyer ◽  
H. Bui ◽  
L. Chou ◽  
J. Evans ◽  
L. C. Keil ◽  
...  

NO synthase is present in magnocellular neurons of supraoptic and paraventricular nuclei as well as in the posterior pituitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chronically prepared rabbits to determine the effect of NO synthesis inhibition with NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) on basal vasopressin secretion and vasopressin responses to increased plasma osmolality (hypertonic saline infusion; P osm) and decreased blood pressure (nitroprusside infusion). L-NAME infusion (0.5 mg.kg-1 x min-1 i.v.) increased mean arterial pressure [MAP; 82.6 +/- 3.4 to 93.0 +/- 3.0 mmHg (P < 0.02)], decreased heart rate [HR; 242 +/- 12 to 209 +/- 9 beats/min (P < 0.02)], decreased plasma renin activity [PRA; 3.1 +/- 0.6 to 2.0 +/- 0.6 ng.ml-.2 h-1 (P < 0.001)], and increased plasma vasopressin concentration [P AVP; 2.2 +/- 0.3 to 4.5 +/- 1.0 pg/ml (P < 0.05)]. P(osm) did not change. Hypertonic saline infusion did not change MAP or HR but decreased PRA [4.3 +/- 0.8 to 0.9 +/- 0.2 ng.ml-1 x 2 h-1 (P < 0.01)], increased P(osm) [284 +/- 1 to 305 +/- 2 mosmol/kg H2O (P < 0.001)], and increased PAVP [2.8 +/- 0.3 to 12.7 +/- 2.7 pg/ml (P < 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 269 (4) ◽  
pp. R874-R880 ◽  
Author(s):  
A. Takamata ◽  
G. W. Mack ◽  
N. S. Stachenfeld ◽  
E. R. Nadel

We examined the effect of increased body core temperature (Tes) on the plasma arginine vasopressin concentration ([AVP]p) and thirst responses to increased plasma osmolality (Posm) induced by 3% NaCl infusion for 120 min in seven healthy humans. Tes was increased by immersion of the lower legs in 41 degrees C water in a 28 degrees C room (passive heating; HT). Immersion of the lower legs in 34.5 degrees C water on a separate day served as the control (thermoneutral; NT). The 120-min hypertonic saline infusion was initiated 30 min after the onset of leg immersion and was followed by a 30-min rehydration period. Tes in HT increased by 0.21 +/- 0.04 degree C before infusion and by 0.86 +/- 0.08 degree C at the end of infusion. The change in Tes in NT before and after the infusion was negligible. Posm was increased by 15.0 +/- 1.0 mosmol/kgH2O by infusion in both NT and HT. [AVP]p increased by 3.48 +/- 0.72 pg/ml in NT and by 7.59 +/- 1.02 pg/ml in HT. Thus the increase in [AVP]p at a given increase in Posm was markedly higher in HT than in NT. The plasma renin activity response to hypertonic saline infusion in both conditions was similar. Subjective thirst rating and cumulative water intake during rehydration were higher in HT than in NT.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 108 (2) ◽  
pp. 309-312 ◽  
Author(s):  
C. Redekopp ◽  
J. H. Livesey ◽  
W. Sadler ◽  
R. A. Donald

ABSTRACT In order to assess the physiological importance of endogenous arginine vasopressin (AVP) in augmenting the ACTH response to corticotrophin-releasing factor (CRF), the response to CRF during hypertonic saline infusion in six Coopworth sheep was examined. A 4-h infusion of 5% (w/v) NaCl (3·8 ml/min) resulted in significantly (P < 0·01) greater rises in ACTH and cortisol, but not aldosterone, than were observed after CRF alone. Infusion of hypertonic saline without CRF resulted in a highly significant (P < 0·001) rise in plasma osmolality and AVP but no significant change in plasma ACTH, cortisol or aldosterone. It is concluded that a marked but physiological increase in peripheral (and presumably central) levels of AVP does not result in any demonstrable change in plasma ACTH concentration. However, under these conditions, the ACTH and cortisol responses to CRF are considerably augmented. J. Endocr. (1986) 108, 309–312


1986 ◽  
Vol 111 (3) ◽  
pp. 495-499
Author(s):  
P. H. Baylis ◽  
C. Pippard ◽  
J. M. Burd

ABSTRACT Infusion of hypertonic saline into six normal volunteers caused an increase in plasma osmolality from 286·8 ± 1·7 (mean ± s.e.m.) to 307·6 ± 2·6 mosmol/kg (P<0·001), a 7·1% increase in estimated blood volume, a rise in plasma immunoreactive arginine vasopressin (AVP) concentrations from 1·3 ± 0·2 to 12·7 ±3·6 pmol/l (P<0·001) but no change in plasma AVP concentrations (2·1 ±0·9 and 1·9 ± 1·3 pmol/l) as measured by a cytochemical technique based on the ability of AVP to stimulate rat renal medullary Na+ /K+-ATPase activity. Addition of synthetic AVP to plasma obtained before, during and after hypertonic saline infusion also failed to stimulate Na+/K+-ATPase activity. The results suggest that infusion of hypertonic saline interfered with the cytochemical assay for AVP by inhibiting AVP-stimulated medullary Na+/K+-ATPase activity. We conclude that the use of this cytochemical method to detect plasma AVP has severe limitations under these experimental conditions. J. Endocr. (1986) 111, 495–499


1980 ◽  
Vol 73 (4) ◽  
pp. 255-260 ◽  
Author(s):  
P H Baylis ◽  
G L Robertson

Hypertonic saline was infused into 11 volunteers to osmotically stimulate vasopressin secretion. A strong positive correlation between plasma arginine vasopressin (PAVP) and plasma osmolality (Pos) was obtained, defined by the function PAVP = 0.63 (Pos – 284), r = +0.80, P < 0.001. The sensitivity of vasopressin secretion to osmotic stimulation was represented by the slope of the expression and the theoretical threshold of vasopressin release by the abscissal intercept. Plasma osmolality at the onset of thirst was 298.5 ± 1.1 mmol/kg. Application of hypertonic saline infusion to 10 polyuric patients clearly separated those with normal osmoregulation of vasopressin secretion from those with cranial diabetes insipidus.


2001 ◽  
Vol 86 (12) ◽  
pp. 5749-5754 ◽  
Author(s):  
Eiji Itagaki ◽  
Sachihiko Ozawa ◽  
Shinya Yamaguchi ◽  
Kenji Ushikawa ◽  
Teruaki Tashiro ◽  
...  

To clarify the mechanism for the potentiation of CRH-induced ACTH response by the infusion of hypertonic saline, we investigated changes in plasma ACTH concentration after infusion of 5% hypertonic saline in five patients with untreated central diabetes insipidus (DI). Basal levels of plasma ACTH and cortisol in the DI group were not significantly different from those in normal control subjects. The infusion of hypertonic saline produced an increase in plasma arginine vasopressin (AVP) in controls, but did not elevate ACTH. However, in patients with DI, the plasma AVP concentration did not change, but circulating ACTH increased 3.6-fold (7.7 ± 1.5 to 23.0 ± 2.7 pmol/liter; P &lt; 0.01), and plasma cortisol also increased significantly (298 ± 99 to 538 ± 124 nmol/liter; P &lt; 0.05). Moreover, a positive correlation was observed between plasma ACTH and osmolality (r = 0.72; P &lt; 0.005). These results indicate that ACTH secretion in DI patients is regulated by a mechanism distinct from that in healthy subjects. It seems possible that the increase in plasma osmolality promotes ACTH secretion in DI patients through AVP and/or urocortin via the hypophyseal portal system, independent of the AVP secretion from magnocellular neurons.


1991 ◽  
Vol 81 (s25) ◽  
pp. 471-476 ◽  
Author(s):  
Felix Vargas ◽  
Maria J. Baz ◽  
Juan de D. Luna ◽  
Jesus Andrade ◽  
Esteban Jodar ◽  
...  

1. Urinary excretion of digoxin-like immunoreactive factor and arginine-vasopressin and other parameters related to salt and water metabolism were studied in hyper- and hypo-thyroid rats after different tests. 2. Urinary excretion of arginine-vasopressin was increased in hyperthyroid and reduced in hypothyroid rats with respect to controls, in response to water deprivation or a hypertonic saline load. 3. Control and hypothyroid rats showed the highest urinary excretion of digoxin-like immunoreactive factor after a hypertonic saline load. However, hyperthyroid rats had the highest urinary levels of digoxin-like immunoreactive factor under normal conditions. 4. From these results it is suggested that: (a) hyper- and hypo-thyroid rats exhibit hyper- and hypo-responsiveness of arginine-vasopressin secretion to osmotic stimuli, respectively; (b) an unidentified digoxin-like immunoreactive factor measured in unextracted rat urine may be related to diuresis and natriuresis in control and hypothyroid rats; however, dissociation between this factor and natriuresis is observed in hyperthyroid rats.


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