Plasma Osmolality of Thirst Onset is Similar to the Threshold for Vasopressin Release in Man

1985 ◽  
Vol 69 (s12) ◽  
pp. 39P-39P ◽  
Author(s):  
C.J. Thompson ◽  
J.M. Burd ◽  
P.H. Baylis
Keyword(s):  
Plasma Osmolality ◽  
Vasopressin Release

scholarly journals Birth elicits a conserved neuroendocrine response with implications for perinatal osmoregulation and neuronal cell death

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yarely C. Hoffiz ◽  
Alexandra Castillo-Ruiz ◽  
Megan A. L. Hall ◽  
Taylor A. Hite ◽  
Jennifer M. Gray ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Surrogate Marker ◽  
Plasma Osmolality ◽  
Neuronal Cell ◽  
Clinical Findings ◽  
Neural Activation ◽  
Vasopressin Release ◽  
Neuroendocrine Response ◽  
The Difference

AbstractLong-standing clinical findings report a dramatic surge of vasopressin in umbilical cord blood of the human neonate, but the neural underpinnings and function(s) of this phenomenon remain obscure. We studied neural activation in perinatal mice and rats, and found that birth triggers activation of the suprachiasmatic, supraoptic, and paraventricular nuclei of the hypothalamus. This was seen whether mice were born vaginally or via Cesarean section (C-section), and when birth timing was experimentally manipulated. Neuronal phenotyping showed that the activated neurons were predominantly vasopressinergic, and vasopressin mRNA increased fivefold in the hypothalamus during the 2–3 days before birth. Copeptin, a surrogate marker of vasopressin, was elevated 30-to 50-fold in plasma of perinatal mice, with higher levels after a vaginal than a C-section birth. We also found an acute decrease in plasma osmolality after a vaginal, but not C-section birth, suggesting that the difference in vasopressin release between birth modes is functionally meaningful. When vasopressin was administered centrally to newborns, we found an ~ 50% reduction in neuronal cell death in specific brain areas. Collectively, our results identify a conserved neuroendocrine response to birth that is sensitive to birth mode, and influences peripheral physiology and neurodevelopment.

Factors associated with vasopressin release in exercising swine

1994 ◽  
Vol 266 (1) ◽  
pp. R118-R124 ◽  
Author(s):  
C. L. Stebbins ◽  
J. D. Symons ◽  
M. D. McKirnan ◽  
F. F. Hwang
Keyword(s):  
Plasma Volume ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Treadmill Running ◽  
Maximal Heart Rate ◽  
Ang Ii ◽  
Strong Correlations ◽  
Vasopressin Release ◽  
Lysine Vasopressin

This study examined the effect of dynamic exercise on vasopressin release in the miniswine and factors that may elicit this response (n = 15). Thus lysine vasopressin (LVP), the catecholamines epinephrine and norepinephrine (EPI and NE), plasma renin activity (PRA), and plasma volume, Na+, and osmolality were measured before and during treadmill running at work intensities of 60, 80, and 100% of each swine's maximal heart rate reserve (HRR). LVP increased in a progressive manner similar to that of humans, ranging from 5.9 +/- 0.4 pg/ml before exercise to 30.1 +/- 4.5 pg/ml during maximal exercise. EPI, NE, and PRA [an index of angiotensin II (ANG II) activity] demonstrated a pattern of response comparable to LVP. Although these hormones can influence the release of LVP, only PRA displayed a strong correlation with LVP (r = 0.84). When ANG II synthesis was blocked (captopril, 1-3 mg/kg, intra-atrial injection) during exercise (80% HRR), plasma LVP was reduced from 9.9 +/- 0.6 to 7.5 +/- 0.6 pg/ml (P < 0.05). In addition, moderate-to-strong correlations were found between plasma concentrations of LVP and plasma osmolality (r = 0.79) and body temperature (r = 0.78). Plasma LVP also correlated with decreases in plasma volume (r = 0.84). These data suggest that the miniswine model is a good one for studying vasopressin effects during exercise and that ANG II appears to be a particularly strong stimulus for the release of this hormone.

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.

Abstract P322: Vasopressin Release is Enhanced Before the Development of Preeclampsia in Humans Despite Exaggerated Suppression of Plasma Osmolality

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Mark K Santillan ◽  
Sabrina M Scroggins ◽  
Alyssa T Ray ◽  
Phillip C Witcher ◽  
Jeremy A Sandgren ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Gestational Age ◽  
Clinical Symptoms ◽  
Freezing Point ◽  
Tissue Bank ◽  
Plasma Osmolality ◽  
Fetal Tissue ◽  
Chronic Hypertension ◽  
Vasopressin Release ◽  
Osmotic Stimuli

Plasma osmolality (Osm) suppression is of critical importance to maintain appropriate blood volume to perfuse the uterus during pregnancy. Osm is reduced starting at the fifth week of gestation via increased arginine vasopressin (AVP) secretion. This increased secretion is maintained via a decrease in the AVP/osmotic release threshold. We previously demonstrated that pregnant women who develop preeclampsia (PreE) exhibit exaggerated AVP secretion as early as the 6th week of gestation via measurement of copeptin, the stable C-terminal fragment of AVP. It is unclear whether AVP secretion is elevated before the onset of PreE due to osmotic or non-osmotic stimuli. We tested the hypothesis that elevated AVP secretion before PreE may be associated with elevated Osm (a strong stimulant of AVP secretion). Plasma and clinical data from pregnant women were obtained from the University of Iowa Maternal-Fetal Tissue Bank (IRB#200910784). Osm was measured using the freezing-point suppression technique. Osm was assessed in non-pregnant women (n=109), pregnant women who later developed PreE (n=12 for 7-12 weeks, n=9 for 16-24 weeks), and maternal and gestational age matched controls (n=25 for 6-13 weeks, n=15 for 14-27 weeks). As expected, Osm was decreased in control pregnancies (non-pregnant 291±1 vs pregnant 286±1 mOsm/kg, p<0.05). Contrary to our hypothesis, the Osm decrease was exaggerated in women who would later develop PreE (1st trimester: PreE 279±4 vs control 287±3, and 2 nd trimester: PreE 277±4 vs control 285±3 mOsm/kg; effect of PreE p<0.05, gestational age p=NS, interaction p=NS) even after controlling for age, BMI, diabetes, chronic hypertension, history of preeclampsia, and gravida (model p<0.05). Despite suppressed Osm, plasma copeptin was elevated in the PreE group at all timepoints (p<0.05). These data support the conclusion that long before the development of clinical symptoms of PreE, the rate of secretion of AVP is inappropriately increased despite maintenance of normal osmotic-regulating actions of AVP. This effect must be the result of increased non-osmotic stimuli for AVP, and a suppression of the AVP/osmotic release threshold beyond that observed in control pregnancies.

Increased plasma osmolality stimulates peripheral and central vasopressin release in male and female rats

1994 ◽  
Vol 267 (4) ◽  
pp. R923-R928 ◽  
Author(s):  
M. Ota ◽  
J. T. Crofton ◽  
H. Liu ◽  
G. Festavan ◽  
L. Share
Keyword(s):  
Interstitial Fluid ◽  
Plasma Osmolality ◽  
Female Rats ◽  
Microdialysis Probe ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Male And Female Rats ◽  
Supraoptic Nuclei

It has been demonstrated that the neurohypophysial hormones can be released intrahypothalamically by the paraventricular (PVN) and supraoptic nuclei. The present experiments were undertaken to determine whether a physiological stimulus for vasopressin release, increased plasma osmolality, will stimulate the release of vasopressin by the PVN into the surrounding interstitial fluid, and whether the responses are affected by gender. Intravenous infusion of 2.5 M NaCl for 60 min (0.1 ml.kg-1.min-1) in conscious rats resulted in an increased vasopressin concentration in the dialysate from a microdialysis probe adjacent to the PVN. This response was greater in nonestrous females than in males. On the other hand, the rise in the plasma vasopressin concentration was greater in males than in nonestrous females. Mean arterial blood pressure increased and heart rate decreased, but these responses were not affected by gender. The role of centrally released vasopressin in the control of the peripheral release of vasopressin is conjectural, but both responses may be modulated by the gonadal steroid hormones.

Thirst and vasopressin release in the dog: an osmoreceptor or sodium receptor mechanism?

1980 ◽  
Vol 238 (5) ◽  
pp. R333-R339 ◽  
Author(s):  
T. N. Thrasher ◽  
C. J. Brown ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Nacl Solution ◽  
Elevated Plasma ◽  
Vasopressin Release ◽  
Hypertonic Glucose ◽  
Hypertonic Solutions ◽  
Vasopressin Secretion ◽  
Plasma Arginine

The effects of intravenous infusion of hypertonic NaCl, sucrose, glucose, urea, or isotonic NaCl solution on thirst and plasma arginine vasopressin concentration (AVP) were studied in five conscious dogs. The changes in osmolality and sodium concentration of plasma and cerebrospinal fluid (CSF) were measured at the threshold of drinking, or after 45 min if no drinking occurred. Hypertonic NaCl and sucrose stimulated drinking in all dogs and significantly elevated plasma AVP. Equally hypertonic glucose, urea, or isotonic NaCl failed to stimulate any drinking or vasopressin secretion. All hypertonic solutions caused significant and similar increases in the osmolality and sodium concentration of CSF. Plasma osmolality was increased by the hypertonic solutions. Plasma sodium was increased by hypertonic NaCl, decreased by sucrose and glucose, and not changed by urea. Isotonic NaCl had no effect on either plasma or CSF composition. These data are not consistent with either a sodium or an osmoreceptor mechanism located within the blood-brain barrier (BBB) or with a peripheral sodium receptor mechanism. An intracranial osmoreceptor located on the blood side of the BBB is proposed to explain these results.

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.

Effects of high altitude and water deprivation on arginine vasopressin release in men

2004 ◽  
Vol 286 (1) ◽  
pp. E20-E24 ◽  
Author(s):  
C. M. Maresh ◽  
W. J. Kraemer ◽  
D. A. Judelson ◽  
J. L. VanHeest ◽  
L. Trad ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Vasopressin Release ◽  
Altitude Exposure ◽  
Blood Pressures ◽  
Healthy Males

High-altitude exposure changes the distribution of body water and electrolytes. Arginine vasopressin (AVP) may influence these alterations. The purpose of this study was to examine the effect of a 24-h water deprivation trial (WDT) on AVP release after differing altitude exposures. Seven healthy males (age 22 ± 1 yr, height 176 ± 2 cm, mass 75.3 ± 1.8 kg) completed three WDTs: at sea level (SL), after acute altitude exposure (2 days) to 4,300 m (AA), and after prolonged altitude exposure (20 days) to 4,300 m (PA). Body mass, standing and supine blood pressures, plasma osmolality (Posm), and plasma AVP (PAVP) were measured at 0, 12, 16, and 24 h of each WDT. Urine volume was measured at each void throughout testing. Baseline Posm increased from SL to altitude (SL 291.7 ± 0.8 mosmol/kgH2O, AA 299.6 ± 2.2 mosmol/kgH2O, PA 302.3 ± 1.5 mosmol/kgH2O, P < 0.05); however, baseline PAVP measurements were similar. Despite similar Posm values, the maximal PAVP response during the WDT (at 16 h) was greater at altitude than at SL (SL 1.7 ± 0.5 pg/ml, AA 6.4 ± 0.7 pg/ml, PA 8.7 ± 0.9 pg/ml, P < 0.05). In conclusion, hypoxia appeared to alter AVP regulation by raising the osmotic threshold and increasing AVP responsiveness above that threshold.

Atrial natriuretic peptide inhibits osmolality-induced arginine vasopressin release in man

1988 ◽  
Vol 75 (1) ◽  
pp. 35-39 ◽  
Author(s):  
M. J. Allen ◽  
V. T. Y. Ang ◽  
E. D. Bennett ◽  
J. S. Jenkins
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Random Order ◽  
Vasopressin Release ◽  
Plasma Arginine ◽  
Placebo Infusion ◽  
Atrial Natriuretic

1. Eight normal volunteers were infused with 5% saline (5 g of NaCl/100 ml) at a rate of 0.06 ml min−1 kg−1 for 120 min to increase plasma osmolality and plasma arginine vasopressin. Human atrial natriuretic peptide (α-hANP; 100 μg) or placebo was given in random order in a double-bind cross-over design for the last 20 min of the saline infusion. 2. Compared with the placebo infusion, atrial natriuretic peptide (ANP) produced a 43% greater sodium excretion and a 34% greater urinary volume in the subsequent hour. 3. Mean plasma immunoreactive ANP did not increase in response to changes in osmolality and rose to a peak of 118 pg/ml during the α-hANP infusion. α-hANP produced significant suppression of mean plasma arginine vasopressin over the 60 min after the infusions. 4. We conclude that ANP is not released in response to increased osmolality in vivo, and that it inhibits osmolality-induced arginine vasopressin release in man.

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