Plasma vasopressin responses in postpartum hypopituitarism: impaired response to osmotic stimuli

1992 ◽  
Vol 127 (6) ◽  
pp. 494-498 ◽  
Author(s):  
MA Arnaout ◽  
K Ajlouni
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Vasopressin ◽  
Basal Plasma ◽  
The Mean ◽  
Thyroxine Replacement Therapy

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.

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
Keyword(s):  
Diabetes Insipidus ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Normal Subjects ◽  
Urine Concentration ◽  
Published Data ◽  
Posterior Pituitary ◽  
Primary Polydipsia ◽  
Number Of Factors

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.

Acute suppression of plasma vasopressin and thirst after drinking in hypernatremic humans

1987 ◽  
Vol 252 (6) ◽  
pp. R1138-R1142 ◽  
Author(s):  
C. J. Thompson ◽  
J. M. Burd ◽  
P. H. Baylis
Keyword(s):  
Sodium Chloride ◽  
Hypertonic Saline ◽  
Analogue Scale ◽  
Chloride Solution ◽  
Sodium Chloride Solution ◽  
Plasma Osmolality ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
The Mean ◽  
Hypertonic Saline Infusion

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)

Oral hypertonic saline causes transient fall of vasopressin in humans

1986 ◽  
Vol 251 (2) ◽  
pp. R214-R217 ◽  
Author(s):  
J. R. Seckl ◽  
T. D. Williams ◽  
S. L. Lightman
Keyword(s):  
Drinking Water ◽  
Plasma Renin Activity ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Total Protein ◽  
Tap Water ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Oral Rehydration ◽  
Plasma Arginine

After dehydration, oral rehydration causes a fall in plasma arginine vasopressin (AVP) that precedes changes in plasma osmolality. To investigate further the stimulus for this effect, its specificity, and association with thirst, six volunteers were deprived of water for 24 h and given a salt load on two separate occasions. On each study day they then drank rapidly 10 ml/kg of either tap water or hypertonic saline (360 mosmol/kg). There was a significant fall in plasma AVP from 2.0 +/- 0.3 to 1.2 +/- 0.4 pmol/l (P less than 0.05) 5 min after drinking water and from 1.8 +/- 0.3 to 0.9 +/- 0.2 pmol/l (P less than 0.05) after hypertonic saline. Plasma osmolality fell 30-60 min after water and was unchanged after saline. Plasma renin activity, oxytocin, and total protein all remained unchanged. All subjects reported diminished thirst after hypertonic saline. Gargling with water reduced thirst but did not affect plasma AVP. There appears to be a drinking-mediated neuroendocrine reflex that decreases plasma AVP irrespective of the osmolality of the liquid consumed. The sensation of thirst did not correlate with plasma osmolality and was not always related to plasma AVP concentration.

Lack of effect of vasopressin replacement on renin hypersecretion in Brattleboro rats

1989 ◽  
Vol 257 (5) ◽  
pp. R1117-R1122
Author(s):  
R. M. Golin ◽  
E. Gotoh ◽  
L. C. Keil ◽  
R. L. Shackelford ◽  
W. F. Ganong
Keyword(s):  
Plasma Renin Activity ◽  
Diabetes Insipidus ◽  
Blood Brain Barrier ◽  
Arginine Vasopressin ◽  
Sympathetic Activity ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Brattleboro Rats ◽  
Plasma Vasopressin ◽  
Long Evans

To determine how the vasopressin deficiency in homozygous Brattleboro rats with diabetes insipidus produces increased renin secretion, homozygous and heterozygous Brattleboro rats were infused through subcutaneously implanted Alzet minipumps for 1 wk with a dose of arginine vasopressin that restored plasma vasopressin to normal in the homozygous animals. In the homozygous animals, plasma renin activity (PRA) and the PRA response to immobilization remained elevated compared with Long-Evans controls. Propranolol reduced PRA to normal and markedly reduced the PRA response to immobilization. PRA was normal in heterozygous Brattleboro rats. The data indicate that the increased renin secretion in homozygous rats is a result of increased sympathetic activity, and because circulating vasopressin does not cross the blood-brain barrier, it seems likely that the increased sympathetic activity is central in origin.

Effect of inhibition of nitric oxide synthesis on vasopressin secretion in conscious rabbits

1994 ◽  
Vol 266 (2) ◽  
pp. H822-H828 ◽  
Author(s):  
M. Goyer ◽  
H. Bui ◽  
L. Chou ◽  
J. Evans ◽  
L. C. Keil ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Posterior Pituitary ◽  
Paraventricular Nuclei ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Posterior Pituitary Gland ◽  
Hypertonic Saline Infusion

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)

Interference in the cytochemical assay of plasma vasopressin by a circulating factor induced by salt-loading in man

1986 ◽  
Vol 111 (3) ◽  
pp. 495-499
Author(s):  
P. H. Baylis ◽  
C. Pippard ◽  
J. M. Burd
Keyword(s):  
Atpase Activity ◽  
Hypertonic Saline ◽  
Blood Volume ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Experimental Conditions ◽  
Salt Loading ◽  
Plasma Vasopressin ◽  
Cytochemical Technique ◽  
Hypertonic Saline Infusion

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

Comparison of the Renin Response to Dopamine and Noradrenaline in Normal Subjects and Patients with Autonomic Insufficiency

1974 ◽  
Vol 46 (4) ◽  
pp. 481-488 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
A. B. Kurtz ◽  
J. D. H. Slater
Keyword(s):  
Autonomic Failure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Control Groups ◽  
Autonomic Reflexes ◽  
Fractional Increase ◽  
The Mean ◽  
Autonomic Insufficiency ◽  
Stimulation Of

1. The effect on plasma renin activity (PRA) of dopamine and noradrenaline infusions was studied in three patients with Shy—Drager syndrome, three patients with Parkinson's disease and normal autonomic reflexes, and three healthy volunteers. The patients with the Shy—Drager syndrome had functional evidence of a peripheral lesion of the sympathetic nervous system and subnormal PRA on a controlled sodium intake. 2. In all subjects catecholamines were infused step-wise for 4 min until a 30% rise in systolic blood pressure occurred. 3. In each subject, PRA fell after noradrenaline but rose after dopamine. The mean fractional increase in PRA after dopamine was no less in the Shy—Drager patients than in the control groups. 4. The results suggest, first, that stimulation of dopamine receptors can release renin, and secondly, that inadequate renin stores cannot explain the low PRA found in our patients with autonomic failure.

scholarly journals Increases in Plasma ACTH and Cortisol after Hypertonic Saline Infusion in Patients with Central Diabetes Insipidus

2001 ◽  
Vol 86 (12) ◽  
pp. 5749-5754 ◽  
Author(s):  
Eiji Itagaki ◽  
Sachihiko Ozawa ◽  
Shinya Yamaguchi ◽  
Kenji Ushikawa ◽  
Teruaki Tashiro ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Plasma Osmolality ◽  
Central Diabetes Insipidus ◽  
Portal System ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Acth Concentration ◽  
Plasma Arginine ◽  
Hypertonic Saline Infusion

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.

Osmoregulation of thirst and vasopressin during normal menstrual cycle

1988 ◽  
Vol 254 (4) ◽  
pp. R641-R647 ◽  
Author(s):  
T. J. Vokes ◽  
N. M. Weiss ◽  
J. Schreiber ◽  
M. B. Gaskill ◽  
G. L. Robertson
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Plasma Osmolality ◽  
Free Water ◽  
Urine Osmolality ◽  
Free Water Clearance ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Normal Menstrual Cycle ◽  
Basal Plasma

Changes in osmoregulation during normal menstrual cycle were examined in 15 healthy women. In 10 women, studied repetitively during two consecutive menstrual cycles, basal plasma osmolality, sodium, and urea decreased by 4 mosmol/kg, 2 meq/l, and 0.5 mM, respectively (all P less than 0.02) from the follicular to luteal phase. Plasma vasopressin, protein, hematocrit, mean arterial pressure, and body weight did not change. In five other women, diluting capacity and osmotic control of thirst and vasopressin release were assessed in follicular, ovulatory, and luteal phases. Responses of thirst and/or plasma vasopressin, urine osmolality, osmolal and free water clearance to water loading, and infusion of hypertonic saline were normal and similar in the three phases. However, the plasma osmolality at which plasma vasopressin and urine osmolality were maximally suppressed as well as calculated osmotic thresholds for thirst and vasopressin release were lower by 5 mosmol/kg in the luteal than in the follicular phase. This lowering of osmotic thresholds for thirst and vasopressin release, which occurs in the luteal phase, is qualitatively similar to that observed in pregnancy and should be taken into account when studying water balance and regulation of vasopressin secretion in healthy cycling women.

Effect of head-down tilt on basal plasma norepinephrine and renin activity in humans

1985 ◽  
Vol 59 (4) ◽  
pp. 1068-1071 ◽  
Author(s):  
S. R. Goldsmith ◽  
G. S. Francis ◽  
J. N. Cohn
Keyword(s):  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Plasma Norepinephrine ◽  
Central Venous ◽  
Basal Plasma ◽  
Cardiopulmonary Baroreceptors

The effects of loading cardiopulmonary baroreceptors on basal norepinephrine and renin activity were studied in six normal subjects. Loading of cardiopulmonary baroreceptors was accomplished by a 60-min 30 degrees head-down tilt with small supplemental saline infusions. Central venous pressure was measured continuously by intrathoracic catheter; arterial pressure was measured indirectly by cuff. During the tilt, central venous pressure increased from 5.1 +/- 1.3 to 8.9 +/- 1.7 mmHg (P less than 0.001), whereas arterial pressure was unchanged. Plasma norepinephrine (185 +/- 85 pg/ml) and plasma renin activity (3.9 +/- 5.7 ng . ml-1 . h-1) did not change. Moderate sustained loading of cardiopulmonary baroreceptors is therefore without effect on unstressed plasma norepinephrine and renin activity in normal humans, suggesting that the tonic inhibitory effects of these receptors on these neurohumoral control systems are not readily increased in the basal state.

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