The physiological significance of arginine vasopressin in potentiating the response to corticotrophin-releasing factor in sheep

1986 ◽  
Vol 108 (2) ◽  
pp. 309-312 ◽  
Author(s):  
C. Redekopp ◽  
J. H. Livesey ◽  
W. Sadler ◽  
R. A. Donald
Keyword(s):  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Physiological Significance ◽  
Plasma Acth ◽  
Physiological Importance ◽  
Corticotrophin Releasing Factor ◽  
Acth Concentration ◽  
Cortisol Responses ◽  
Hypertonic Saline Infusion

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

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.

Regulation of vasopressin secretion in a patient with chronic hypernatraemia

1985 ◽  
Vol 110 (3) ◽  
pp. 346-351 ◽  
Author(s):  
Simon Smitz ◽  
Jean-Jacques Legros
Keyword(s):  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Concomitant Increase ◽  
Specific Radioimmunoassay ◽  
Vasopressin Secretion ◽  
Plasma Arginine ◽  
The Brain ◽  
Unrestricted Diet ◽  
Hypertonic Saline Infusion

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.

Vasopressin responses to corticotropin releasing factor and hyperosmolality in conscious dogs

1986 ◽  
Vol 251 (6) ◽  
pp. R1235-R1239
Author(s):  
H. Raff ◽  
M. M. Skelton ◽  
D. C. Merrill ◽  
A. W. Cowley
Keyword(s):  
Hypertonic Saline ◽  
Plasma Osmolality ◽  
Corticotropin Releasing Factor ◽  
Saline Infusion ◽  
Conscious Dogs ◽  
Plasma Sodium ◽  
Plasma Vasopressin ◽  
Cortisol Responses ◽  
Osmotic Stimulus ◽  
Hypertonic Saline Infusion

We recently reported that ovine corticotropin releasing factor (CRF) infusion in conscious dogs elevated plasma vasopressin. The present study examines the vasopressin, adrenocorticotropic hormone (ACTH), and cortisol responses to CRF infusion (20 ng X kg-1 X min-1), to hypertonic saline infusion (NaCl 0.054 meq X kg-1 X min-1), and to simultaneous coinfusion of CRF and NaCl (CRF + NaCl) without (no-dex) or with (dex-treated) dexamethasone pretreatment in six conscious dogs (6-8 experiments/dog). CRF had no significant effect on plasma sodium or osmolality, blood pressure, or heart rate. NaCl increased plasma sodium from 146 +/- 1 to 151 +/- 1 meq/l and plasma osmolality from 298 +/- 3 to 305 +/- 3 mosmol/kg. Vasopressin increased significantly during CRF (2.1 +/- 0.5 to 4.8 +/- 1.1 pg/ml) and NaCl (1.9 +/- 0.3 to 5.0 +/- 0.8 pg/ml). Coinfusion of CRF and NaCl resulted in a response larger than the sum of the two infusions alone (3.0 +/- 1.6 to 31.4 +/- 18.5 pg/ml). The ACTH response to CRF (45 +/- 8 to 288 +/- 88 pg/ml) was not augmented by coinfusion with NaCl. DEX attenuated the vasopressin and ACTH responses to each infusion. We conclude that CRF-induced increases in vasopressin are augmented by a simultaneous osmotic stimulus. In addition, the plasma vasopressin responses to CRF and/or hypertonic saline infusion are inhibited by glucocorticoid pretreatment.

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

Inappropriate vasopressin secretion in two dogs

1988 ◽  
Vol 117 (1) ◽  
pp. 59-64 ◽  
Author(s):  
A. Rijnberk ◽  
W. J. Biewenga ◽  
J. A. Mol
Keyword(s):  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
High Plasma ◽  
The Other ◽  
Normal Response ◽  
Vasopressin Secretion ◽  
Low Threshold ◽  
Normal Sensitivity ◽  
Hypertonic Saline Infusion

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.

Reproducibility of osmotic and nonosmotic tests of vasopressin secretion in men

1991 ◽  
Vol 260 (3) ◽  
pp. R533-R539 ◽  
Author(s):  
C. J. Thompson ◽  
P. Selby ◽  
P. H. Baylis
Keyword(s):  
Blood Glucose ◽  
Linear Regression ◽  
Hypertonic Saline ◽  
Linear Regression Analysis ◽  
Plasma Osmolality ◽  
Saline Infusion ◽  
Intraindividual Variation ◽  
Insulin Tolerance ◽  
Vasopressin Secretion ◽  
Hypertonic Saline Infusion

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.

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)

Abnormalities in the response of plasma arginine vasopressin during hypertonic saline infusion in patients with eating disorders

1989 ◽  
Vol 26 (1) ◽  
pp. 73-86 ◽  
Author(s):  
J.Ken Nishita ◽  
Everett H. Ellinwood ◽  
W.J.Kenneth Rockwell ◽  
Cynthia M. Kuhn ◽  
Graham W. Hoffman ◽  
...  
Keyword(s):  
Eating Disorders ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Saline Infusion ◽  
Plasma Arginine ◽  
Hypertonic Saline Infusion

scholarly journals Fos, RVLM-projecting neurons, and spinally projecting neurons in the PVN following hypertonic saline infusion

2003 ◽  
Vol 284 (4) ◽  
pp. R945-R953 ◽  
Author(s):  
A. Kantzides ◽  
E. Badoer
Keyword(s):  
Spinal Cord ◽  
Hypertonic Saline ◽  
Paraventricular Nucleus ◽  
Cell Activation ◽  
Plasma Osmolality ◽  
Ventrolateral Medulla ◽  
Intravenous Cannula ◽  
Conscious Rats ◽  
Anterior Posterior ◽  
Hypertonic Saline Infusion

Hypertonic saline (HTS; 1.7 M) infused intravenously into conscious rats increases the production of Fos, a marker of cell activation, in the hypothalamic paraventricular nucleus (PVN). The parvocellular PVN contains subpopulations of neurons. However, which subpopulations are activated by HTS is unknown. We determined whether PVN neurons that innervate the rostral ventrolateral medulla (RVLM) or the spinal cord (important autonomic sites) expressed Fos following HTS. Experiments were performed 24–96 h after chronic implantation of an intravenous cannula. HTS significantly increased the number of Fos-positive cells. In the parvocellular PVN, the maximum number of Fos-positive cells occurred rostral of the anterior-posterior level at which the number of neurons that projected to the medulla or spinal cord peaked. Compared with controls, HTS did not significantly increase the number of double-labeled neurons. These findings demonstrate that an elevation in plasma osmolality activates PVN neurons but not the subgroups of PVN neurons with projections to the RVLM or to the spinal cord.

Dexamethasone inhibits ovine corticotrophin-releasing factor (oCRF), arginine vasopressin (AVP), and oCRF + AVP stimulated release of ACTH during the last third of pregnancy in the sheep fetus

1987 ◽  
Vol 65 (6) ◽  
pp. 1186-1192 ◽  
Author(s):  
Laurie J. Norman ◽  
John R. G. Challis
Keyword(s):  
Negative Feedback ◽  
Arginine Vasopressin ◽  
Late Pregnancy ◽  
Feedback Effect ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Corticotrophin Releasing Factor ◽  
Basal Release ◽  
Sheep Fetus ◽  
Acth Release

We examined the hypothesis that in fetal sheep during late pregnancy exogenous glucocorticoids might affect differentially the pituitary response, measured as changes in plasma ACTH concentrations, to the systemic administration of ovine corticotrophin-releasing factor (oCRF), arginine vasopressin (AVP), or oCRF + AVP. At d 113–116 of pregnancy, equimolar injections of oCRF and AVP given separately provoked similar significant increases in plasma ACTH; the change in ACTH over basal values was significantly greater than the sum of the two separate responses when AVP + oCRF were given together. Exogenous dexamethasone did not affect basal ACTH concentrations, but suppressed significantly the responses to oCRF, AVP, and oCRF + AVP. At d 126–130, there was a significant ACTH response to CRF alone and to AVP + oCRF, but not to AVP alone. The response during the first 30 min postinjection to oCRF was significantly less than that to AVP + oCRF. Plasma Cortisol rose after each peptide injection. Exogenous dexamethasone suppressed both basal and stimulated responses to each peptide. At the amounts injected, there was no significant ACTH or Cortisol response to oCRF, AVP, or oCRF + AVP at d 136–140, but dexamethasone suppressed basal ACTH and Cortisol concentrations at this time. We conclude that stimulated, but not basal, release of ACTH is subject to the negative feedback effect of exogenous glucocorticoid by d 113–116 of gestation in fetal sheep. Both basal and stimulated release of ACTH and Cortisol are suppressed after d 125. At the amount of exogenous dexamethasone given, oCRF, AVP, and oCRF + AVP-stimulated responses are affected similarly. Our results suggest different controls of basal and stimulated ACTH release from the pituitary at d 113–116 of gestation. Our findings would be consistent with the pituitary as a level of action for the negative feedback effect of corticosteroids on stimulated ACTH release throughout the last third of pregnancy in fetal sheep.

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