Cellular dehydration acutely degrades mood mainly in women: a counterbalanced, crossover trial

2020 ◽  
pp. 1-9
Author(s):  
HyunGyu Suh ◽  
Harris R. Lieberman ◽  
Lisa T. Jansen ◽  
Abigail T. Colburn ◽  
J. D. Adams ◽  
...  
Keyword(s):  
Heat Exposure ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Acute Effect ◽  
Short Version ◽  
Female Age ◽  
Cellular Dehydration ◽  
Total Mood Disturbance ◽  
Control Plasma ◽  
Total Mood Disturbance Score

Abstract It is unclear if mild-to-moderate dehydration independently affects mood without confounders like heat exposure or exercise. This study examined the acute effect of cellular dehydration on mood. Forty-nine adults (55 % female, age 39 (sd 8) years) were assigned to counterbalanced, crossover trials. Intracellular dehydration was induced with 2-h (0·1 ml/kg per min) 3 % hypertonic saline (HYPER) infusion or 0·9 % isotonic saline (ISO) as a control. Plasma osmolality increased in HYPER (pre 285 (sd 3), post 305 (sd 4) mmol/kg; P < 0·05) but remained unchanged in ISO (pre 285 (sd 3), post 288 (sd 3) mmol/kg; P > 0·05). Mood was assessed with the short version of the Profile of Mood States Questionnaire (POMS). The POMS sub-scale (confusion-bewilderment, depression-dejection, fatigue-inertia) increased in HYPER compared with ISO (P < 0·05). Total mood disturbance score (TMD) assessed by POMS increased from 10·3 (sd 0·9) to 16·6 (sd 1·7) in HYPER (P < 0·01), but not in ISO (P > 0·05). When TMD was stratified by sex, the increase in the HYPER trial was significant in females (P < 0·01) but not in males (P > 0·05). Following infusion, thirst and copeptin (surrogate for vasopressin) were also higher in females than in males (21·3 (sd 2·0), 14·1 (sd 1·4) pmol/l; P < 0·01) during HYPER. In conclusion, cellular dehydration acutely degraded specific aspects of mood mainly in women. The mechanisms underlying sex differences may be related to elevated thirst and vasopressin.

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

Physiological mechanisms for thirst in the nonhuman primate

1982 ◽  
Vol 242 (5) ◽  
pp. R423-R428 ◽  
Author(s):  
R. J. Wood ◽  
E. T. Rolls ◽  
B. J. Rolls
Keyword(s):  
Nonhuman Primate ◽  
Rhesus Monkeys ◽  
Water Deprivation ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Physiological Mechanisms ◽  
Cellular Dehydration ◽  
Primary Determinant ◽  
The Relationship ◽  
Intravenous Sodium

The relationship between body fluid deficits and drinking has been investigated in a nonhuman primate. Intravenous sodium chloride infusions (0.93-3.25 M) given to rhesus monkeys caused drinking correlated with increases in plasma osmolality and sodium concentrations. Sucrose infusions (0.3 M in 0.15 M NaCl) also caused drinking while equiosmolal urea infusions did not. It was found that the drinking threshold corresponded to a 2.3% increase in plasma osmolality. Water deprivation for 24 h caused significant cellular dehydration, as indicated by a 5.8% elevation in plasma osmolality that exceeded the threshold for thirst, and a significant hypovolemia as indicated by elevated plasma protein and hematocrit values. Intravenous water preloads decreased plasma osmolality and produced a dose-related decrease in subsequent drinking. Infusions that restored plasma osmolality to predeprivation values, reduced intake by 85%. Intravenous isotonic saline preloads which abolished the hypovolemia did not have a consistent effect and reduced mean water intakes by only 3.2%. Thus in the rhesus monkey, cellular dehydration is an effective stimulus for thirst, and it is the primary determinant of drinking after water deprivation, used as an example of a natural thirst stimulus. In contrast to findings in nonprimates, the extracellular deficit contributes very little to drinking after water deprivation.

Osmotic and volaemic regulation of atrial and ventricular natriuretic peptide secretion in conscious eels

1996 ◽  
Vol 149 (3) ◽  
pp. 441-447 ◽  
Author(s):  
H Kaiya ◽  
Y Takei
Keyword(s):  
Natriuretic Peptide ◽  
Blood Volume ◽  
Bolus Injection ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Cellular Dehydration ◽  
Ventral Aorta ◽  
Peptide Secretion ◽  
Osmotic Stimuli ◽  
Ventricular Natriuretic Peptide

Abstract The effects of acute manipulation of plasma osmolality and blood volume on plasma atrial and ventricular natriuretic peptide (ANP and VNP) levels were examined in conscious freshwater eels, Anguilla japonica. A bolus injection of hypertonic NaCl (0·85 m and 1·7 m, 2·5 ml/kg body weight) through a catheter into the ventral aorta produced increases in plasma Na concentration and osmolality with parallel concentration-dependent, transient increases in plasma ANP and VNP levels. Plasma ANP and VNP levels also increased after injection of 1·7 m mannitol solution which produced an increase in plasma osmolality but a decrease in plasma Na concentration. However, injection of a 2·0 m solution of urea, which does not cause cellular dehydration in mammals, produced only small increases in plasma ANP and VNP levels, although plasma osmolality increased. A bolus injection of 10 or 25 ml/kg isotonic saline supplemented with 2% dextran for colloidal osmotic pressure, which theoretically increased blood volume by 29% or 71%, produced volume-dependent, transient increases in plasma ANP and VNP levels without changes in plasma Na concentration and osmolality. Similar volume expansion with dialysed eel plasma caused greater increases than with dextran-saline. However, these increases were much smaller than those after osmotic stimuli. These results indicate that secretion of ANP and VNP is regulated by two receptor mechanisms: osmoreceptors activated by cellular dehydration, not specifically by hypernatraemia, and volume or stretch receptors activated by hypervolaemia. The relative importance of the osmoreceptive mechanism is greater in eels than in mammals where volaemic regulation dominates over osmotic regulation for ANP secretion. Journal of Endocrinology (1996) 149, 441–447

Plasma volume during stress in man: osmolality and red cell volume

1979 ◽  
Vol 47 (5) ◽  
pp. 1031-1038 ◽  
Author(s):  
J. E. Greenleaf ◽  
V. A. Convertino ◽  
G. R. Mangseth
Keyword(s):  
Cell Volume ◽  
Plasma Volume ◽  
Heat Exposure ◽  
Plasma Osmolality ◽  
Red Cell ◽  
Short Term ◽  
Red Cell Volume ◽  
Altitude Exposure ◽  
Periods Of Stress

Our purpose was 1) to test the hypothesis that in man there is a range of plasma osmolality within which the red cell volume (RCV) and mean corpuscular volume (MCV) remain essentially constant and 2) to determine the upper limit of this range. During a variety of stresses--submaximal and maximal exercise, heat and altitude exposure, +Gz acceleration, and tilting--changes in plasma osmolality between -1 and +13 mosmol/kg resulted in essentially no change in the regression of percent change in plasma volume (PV) calculated from a change in hematocrit (Hct) on that calculated from a change in Hct + hemoglobin (Hb), i.e., the RCV and MCV were constant. Factors that do not influence RCV are the level of metabolism, heat exposure at rest, and short-term orthostasis (heat-to-foot acceleration). Factors that may influence RCV are exposure to high altitude and long-term orthostasis (head-up tilting). Factors that definitely influence RCV are prior dehydration and extended (greater than 2 h) periods of stress. Thus, either the Hct or the Hct + Hb equations can be used to calculate percent changes in PV under short-term (less than 2 h) periods of stress when the change in plasma osmolality is less than 13 mosmol/kg.

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.

Fluid retention after oral loading with water or saline in camels

1992 ◽  
Vol 262 (5) ◽  
pp. R915-R920 ◽  
Author(s):  
S. Benlamlih ◽  
K. Dahlborn ◽  
R. Z. Filali ◽  
J. Hossaini-Hilali
Keyword(s):  
Body Weight ◽  
Plasma Proteins ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
The Body ◽  
Plasma Aldosterone Concentration ◽  
Excess Water ◽  
Saline Loading ◽  
Long Time

When dehydrated camels are offered water they drink volumes of water exceeding their body water loss during the water deprivation period. The excess water is excreted during 2-4 days. To investigate the ability to retain fluid in the body, normohydrated camels were loaded with water or isotonic saline (0.1 l/kg body wt) by esophageal tube. After water loading plasma osmolality decreased and a water diuresis was seen, but it took 3 days until the body weight returned to prehydration level. Plasma aldosterone concentration (PAC) increased, but plasma renin activity (PRA) and plasma atrial natriuretic peptide (ANP) concentration did not change. After the saline loading plasma osmolality increased and total plasma proteins and hematocrit decreased. Renal Na excretion increased 4 h after the saline load, but the magnitude of the natriuresis was small, and the camels had not regained their body weight 6 days after the load. PAC and PRA decreased after saline loading, while plasma ANP concentration did not change. These data show that camels are able to retain excess water within the body and to tolerate blood hyposmolality for a relatively long time. With saline the retention of fluid lasts even longer despite an attenuation of PAC.

Expression of osmotic stress-related genes in tissues of normal and hyposmotic rats

2003 ◽  
Vol 285 (4) ◽  
pp. F688-F693 ◽  
Author(s):  
Zheng Zhang ◽  
Joan D. Ferraris ◽  
Heddwen L. Brooks ◽  
Ioana Brisc ◽  
Maurice B. Burg
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factor ◽  
Mrna Expression ◽  
Plasma Osmolality ◽  
Hsp 70 ◽  
Taurine Transporter ◽  
Osmolyte Accumulation ◽  
Organic Osmolyte ◽  
Stress Related Genes ◽  
Control Plasma

TonEBP is a transcription factor that, when activated by hypertonicity, increases transcription of genes, including those involved in organic osmolyte accumulation. Surprisingly, it is expressed in virtually all tissues, including many never normally exposed to hypertonicity. We measured TonEBP mRNA (real-time PCR) and protein (Western blot analysis) in tissues of control (plasma osmolality 294 ± 1 mosmol/kgH2O) and hyposmotic (dDAVP infusion plus water loading for 3 days, 241 ± 2 mosmol/kgH2O) rats to test whether the ubiquitous expression of TonEBP mRNA is osmotically regulated around the normal plasma osmolality. TonEBP protein is reduced by hyposmolality in thymus and liver, but not in brain, and is not detected in heart and skeletal muscle. TonEBP mRNA decreases in brain and liver but is unchanged in other tissues. There are no general changes in mRNA of TonEBP-mediated genes: aldose reductase (AR) does not change in any tissue, betaine transporter (BGT1) decreases only in liver, taurine transporter (TauT) only in brain and thymus, and inositol transporter (SMIT) only in skeletal muscle and liver. Heat shock protein (Hsp)70–1 and Hsp70–2 mRNA increase greatly in most tissues, which cannot be attributed to decreased TonEBP activity. The conclusions are as follows: 1) TonEBP protein or mRNA expression is reduced by hyposmolality in thymus, liver, and brain. 2) TonEBP protein and mRNA expression are differentially regulated in some tissues. 3) Although AR, SMIT, BGT1, and TauT are regulated by TonEBP in renal medullary cells, other sources of regulation may predominate in other tissues. 4) TonEBP abundance and activity are regulated by factors other than tonicity in some tissues.

Drinking and natriuresis during volume expansion and intracranial angiotensin or carbachol

1986 ◽  
Vol 251 (2) ◽  
pp. R381-R387
Author(s):  
D. A. Fitts ◽  
J. B. Simpson
Keyword(s):  
Body Fluid ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
The Body ◽  
Ang Ii ◽  
Elevated Plasma ◽  
Precipitous Decline ◽  
Infusion Period ◽  
Drinking Fluid

Two methods of sodium loading were used to counteract the body fluid dilution resulting from natriuresis and water drinking during sustained lateral ventricular infusions of carbachol (CBC) or angiotensin II (ANG II) in rats. It was expected that preventing dilution would also prevent the precipitous decline of both drinking and natriuresis during the later hours of CBC infusion. In the first study, rats having isotonic saline as the sole drinking fluid during CBC infusions drank less fluid and had only slightly higher plasma osmolality and sodium concentration than rats drinking water, which showed extreme dilution. In the second study, rats with only water to drink were given intravenous infusions of 0.15, 0.45, or 1.00 M NaCl solutions at 1.8 ml/h concurrently with the intraventricular infusions. Significant dilution of plasma was found at the two lower rates but not at 1.00 M NaCl in CBC-infused rats. Only the latter group showed both persistent drinking and natriuresis throughout the 4-h infusion period, and this was not because of elevated plasma osmolality. Infusions of ANG II generated less severe body fluid dilution and more persistent drinking in both experiments. The study demonstrates that body fluid dilution may control the offset of both drinking and natriuresis during sustained infusions of CBC and that the more persistent drinking to ANG II vs. CBC probably occurs because of a lesser natriuresis and consequent fluid dilution.

scholarly journals Thermal dehydration-induced thirst in spontaneously hypertensive rats

1999 ◽  
Vol 276 (5) ◽  
pp. R1302-R1310 ◽  
Author(s):  
Christopher C. Barney ◽  
Gina L. Smith ◽  
Michael M. Folkerts
Keyword(s):  
Water Status ◽  
Heat Exposure ◽  
Plasma Osmolality ◽  
Thermal Response ◽  
Hemoglobin Concentration ◽  
Water Losses ◽  
Evaporative Water ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

Spontaneously hypertensive (SH) rats and normotensive Wistar-Kyoto (WKY) rats were exposed to either 25 or 37.5°C for 3.5 h, and their thermal and water balance responses were compared. After exposure, either a blood sample was obtained or the rats were allowed to rehydrate for 4 h. SH rats had both higher core temperatures and evaporative water losses during heat exposure. Measurements of hematocrit, hemoglobin concentration, plasma protein and sodium concentrations, and plasma osmolality indirectly showed that the SH rats were dehydrated relative to the WKY rats after exposure to either 25 or 37.5°C. SH rats drank significantly more water but also had significantly higher urine volumes than the WKY rats and thus rehydrated only slightly better than the WKY rats. SH and WKY rats had similar levels of water intake and urine output after 24 h of water deprivation. The elevated thermal response of SH rats to heat exposure does not appear to lead to uncompensatable changes in body water status.

Hypothalamic thermal stimulation modulates vasopressin release in hyperosmotically stimulated rabbits

1994 ◽  
Vol 267 (4) ◽  
pp. R1089-R1097 ◽  
Author(s):  
R. Keil ◽  
R. Gerstberger ◽  
E. Simon
Keyword(s):  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Significant Rise ◽  
Hypertonic Solution ◽  
Temperature Plasma ◽  
Evaporative Water ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Hypothalamic Control ◽  
Hypertonic Stimulation

Under thermoneutral conditions conscious rabbits received systemic infusions of NaCl as hypertonic solution (90 mueq.min-1.kg body wt-1), which raised their plasma osmolality from 283 to 312 mosmol/kgH2O. Rabbits receiving isotonic saline served as controls. Hypertonic stimulation induced a 60% reduction of both respiratory frequency and evaporative water loss. Rectal temperature rose by 0.4 degrees C despite enhanced peripheral vasodilation as indicated by increased ear skin temperature. Plasma vasopressin (AVP), aldosterone (ALDO), and corticosterone (COR) were significantly elevated from 6 to 16 pg/ml, 90 to 180 pg/ml, and 17 to 40 ng/ml, respectively. To elucidate the importance of central temperature for AVP and adrenal corticosteroid release, hypothalamic thermal stimulations (20 min) were superimposed during established iso- and hyperosmotic steady-state conditions. Different from isosmotic controls, hyperosmotic animals responded to hypothalamic cooling (37 degrees C) with a significant decrease in plasma AVP from 16 to 13 pg/ml and to hypothalamic warming (41 degrees C) with a significant rise from 16 to 19 pg/ml. A weak temperature effect on COR release was also disclosed, especially of hypothalamic cooling, which significantly lowered plasma COR from 42 to 34 ng/ml. These results provide evidence for positive local temperature coefficients of hypothalamic control of AVP release and suggest a similar property also for the control of COR release by the hypothalamo-adenohypophysial axis.

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