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.

scholarly journals Effects of intrathecal kynurenate on arterial pressure during chronic osmotic stress in conscious rats

2013 ◽  
Vol 304 (2) ◽  
pp. H303-H310 ◽  
Author(s):  
Britta Veitenheimer ◽  
John W. Osborn
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Osmotic Stress ◽  
Glutamate Receptors ◽  
Kynurenic Acid ◽  
Plasma Osmolality ◽  
Ventrolateral Medulla ◽  
Neurogenic Hypertension ◽  
Conscious Rats ◽  
Salt Hypertension

Increased plasma osmolality elevates mean arterial pressure (MAP) through activation of the sympathetic nervous system, but the neurotransmitters released in the spinal cord to regulate MAP during osmotic stress remain unresolved. Glutamatergic neurons of the rostral ventrolateral medulla project to sympathetic preganglionic neurons in the spinal cord and are likely activated during conditions of osmotic stress; however, this has not been examined in conscious rats. This study investigated whether increased MAP during chronic osmotic stress depends on activation of spinal glutamate receptors. Rats were chronically instrumented with an indwelling intrathecal (i.t.) catheter for antagonist delivery to the spinal cord and a radiotelemetry transmitter for continuous monitoring of MAP and heart rate. Osmotic stress induced by 48 h of water deprivation (WD) increased MAP by ∼15 mmHg. Intrathecal kynurenic acid, a nonspecific antagonist of ionotropic glutamate receptors, decreased MAP significantly more after 48 h of WD compared with the water-replete state. Water-deprived rats also showed a greater fall in MAP in response to i.t. 2-amino-5-phosphonovalerate. Finally, i.t. kynurenic acid also decreased MAP more in an osmotically driven model of neurogenic hypertension, the DOCA-salt rat, compared with normotensive controls. Our results suggest that spinally released glutamate mediates increased MAP during 48-h WD and DOCA-salt hypertension.

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 < 0.01), and plasma cortisol also increased significantly (298 ± 99 to 538 ± 124 nmol/liter; P < 0.05). Moreover, a positive correlation was observed between plasma ACTH and osmolality (r = 0.72; P < 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.

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 and chronic increases in osmolality increase excitatory amino acid drive of the rostral ventrolateral medulla in rats

2004 ◽  
Vol 287 (6) ◽  
pp. R1359-R1368 ◽  
Author(s):  
Virginia L. Brooks ◽  
Korrina L. Freeman ◽  
Theresa L. O’Donaughy
Keyword(s):  
Amino Acid ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Excitatory Amino Acid ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Saline Infusion ◽  
Ventrolateral Medulla ◽  
Depressor Response ◽  
Hypertonic Saline Infusion

Water deprivation is associated with increased excitatory amino acid (EAA) drive of the rostral ventrolateral medulla (RVLM), but the mechanism is unknown. This study tested the hypotheses that the increased EAA activity is mediated by decreased blood volume and/or increased osmolality. This was first tested in urethane-anesthetized rats by determining whether bilateral microinjection of kynurenate (KYN, 2.7 nmol) into the RVLM decreases arterial pressure less in water-deprived rats after normalization of blood volume by intravenous infusion of isotonic saline or after normalization of plasma osmolality by intravenous infusion of 5% dextrose in water (5DW). Water-deprived rats exhibited decreased plasma volume and elevated plasma osmolality, hematocrit, and plasma sodium, chloride, and protein levels (all P < 0.05). KYN microinjection decreased arterial pressure by 24 ± 2 mmHg ( P < 0.05; n = 17). The depressor response was not altered following isotonic saline infusion but, while still present ( P < 0.05), was reduced ( P < 0.05) to −13 ± 2 mmHg soon after 5DW infusion. These data suggest that the high osmolality, but not low blood volume, contributes to the KYN depressor response. To further investigate the action of increased osmolality on EAA input to RVLM, water-replete rats were also studied after hypertonic saline infusion. Whereas KYN microinjection did not decrease pressure immediately following the infusion, a depressor response gradually developed over the next 3 h. Lumbar sympathetic nerve activity also gradually increased to up to 167 ± 19% of control ( P < 0.05) 3 h after hypertonic saline infusion. In conclusion, acute and chronic increases in osmolality appear to increase EAA drive of the RVLM.

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)

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.

scholarly journals Hypertonic Saline Infusion Acutely Degrades Mood in Healthy Volunteers (P23-014-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
HyunGyu Suh ◽  
Harris Lieberman ◽  
Lisa Jansen ◽  
J D Adams ◽  
Adam Seal ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Mood State ◽  
Surrogate Marker ◽  
Plasma Osmolality ◽  
Acute Effect ◽  
Saline Infusion ◽  
Short Version ◽  
Before And After ◽  
Underlying Mechanisms ◽  
Hypertonic Saline Infusion

Abstract Objectives Mild and moderate dehydration adversely affect mood and cognitive function. During dehydration, hypertonic hypovolemia activates both osmo- and baro-receptors but it is not known which physiological pathway is associated with degraded mood state. This study examined the acute effect of osmoreceptor stimulation on mood. Methods Sixty healthy adults (50% females, 30 ± 1 y; BMI: 26.9 ± 4.0 kg·m−2) were infused intravenously with 3.0% (HYPER) or 0.9% (ISO) NaCl for 2 h (0.1 ml·kg−1·min−1) using a counterbalanced, crossover design. Blood samples were collected every 30 minutes to measure plasma osmolality (POsm), copeptin (a surrogate marker of vasopressin), and renin-angiotensin-aldosterone system (RAAS) hormones. Mood was assessed with the short version of Profile of Mood State (POMS) questionnaire before and after the infusion. Results POsm and copeptin increased from 286 ± 3 mmol·kg−1 to 305 ± 4 mmol·kg−1 and from 4.5 ± 3.7 pmol·L−1 to 20.4 ± 12.8 pmol·L−1, respectively in HYPER (P < 0.05), and were unchanged in ISO (P > 0.05). No hormonal differences were observed between trials for RAAS hormones (P > 0.05). During HYPER copeptin, following the 2-h infusion, was greater in females than in males (female: 23.4 ± 13.9 pmol·L−1, male: 17.4 ± 10.9 pmol·L−1; P < 0.05). The POMS total mood disturbance (TMD) score increased from 10.5 ± 0.9 to 16.5 ± 1.6 in HYPER (P < 0.05), but not in ISO (P > 0.05). Among POMS subscales, depression-dejection and fatigue-inertia increased in HYPER compared to ISO (P < 0.05). When TMD responses in the HYPER trial were analyzed with sex as a between-subjects factor, the increase was significant in females (pre: 10.2 ± 1.0, post: 18.6 ± 2.3; P < 0.001) but not in males (pre: 10.8 ± 1.4, post: 14.0 ± 2.0; P > 0.05). The confusion-bewilderment subscales and fatigue-inertia of the POMS were also elevated post HYPER in females (P < 0.05), but not in ISO (P > 0.05) in either sex. Conclusions Hypertonic saline infusion acutely degrades mood state, and women appear to have a more pronounced response. The underlying mechanisms remain to be determined but may be related to higher copeptin levels in women. The study was registered at ClinicalTrials.gov as NCT02761434. Funding Sources Danone Research. Supporting Tables, Images and/or Graphs

Thirst and fluid regulatory responses to hypertonicity in older adults

1996 ◽  
Vol 271 (3) ◽  
pp. R757-R765 ◽  
Author(s):  
N. S. Stachenfeld ◽  
G. W. Mack ◽  
A. Takamata ◽  
L. DiPietro ◽  
E. R. Nadel
Keyword(s):  
Older Adults ◽  
Hypertonic Saline ◽  
Rating Scale ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Free Water ◽  
Saline Infusion ◽  
Renal Handling ◽  
Aging Adults ◽  
Hypertonic Saline Infusion

To assess the fluid regulatory responses in aging adults, we measured thirst perception and osmoregulation during and after infusion of hypertonic NaCl) saline in older (72 +/- 2 yr, n = 6) and younger (26 +/- n = 6) subjects. Hypertonic saline was infused at 0.1 min-1.kg-1 for 120 min. On a separate day, the same subjects were infused identically with isotonic saline as a control. After infusion and a 30-min equilibration period, the drank water ad libitum for 180 min. Hypertonic infusion led to graded increases in plasma osmolality (Posm; 18 +/- 2 and 20 +/- 2 mosmol/kgH2O) and percent changes plasma volume (16.2 +/- 1.9 and 18.0 +/- 1.2%) that were in older and younger subjects. Osmotically stimulated increases in thirst (94.8 +/- 18.9 and 88.3 +/- 25.6 mm), assessed on a line rating scale, and plasma arginine vasopressin concentration (6.08 +/- 1.50 and 4.51 +/- 1.37 pg/ml, for older younger, respectively) were also unaffected by age. subsequent hypervolemia, both groups of subjects sufficient water to restore preinfusion levels of Posm. Renal handling of free water and sodium was also unaffected by age during recovery from hypertonic saline infusion, but was significantly lower in older subjects during recovery from saline infusion, resulting in net fluid retention and a significant fall in Posm (6 mosmol/kgH2O). In contrast to earlier reports of a blunted thirst response to dehydration hypertonicity, we found that osmotically stimulated thirst and renal osmoregulation were intact in older adults after hypertonic saline infusion.

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