Plasma Vasopressin Levels Research Articles

Factors Relating to the Vertigo Control and Hearing Changes Following Intratympanic Gentamicin for Intractable Ménière's Disease

To look for factors relating to the vertigo control and hearing changes after intratympanic injections of gentamicin (GM). Prospective. Tertiary referral medical center. Twenty-eight patients with intractable Ménière's disease. Three intratympanic injections of GM (once per day for three consecutive days). Although five patients needed further GM injections or vestibular neurectomy because of poor control (Group I), 23 patients had their vertigo controlled for more than two years without further treatment (Group II). The number of vertigo spells per month, pure-tone audiometry, electrocochleography, caloric response, post-head shake nystagmus, and plasma vasopressin as a stress marker were examined. Before GM injections, there was no difference in the number of vertigo spells per month between Groups I and II. However, the hearing thresholds were higher in Group I. Hearing improvement, increase in percentage of canal paresis and induction of post-head shake nystagmus were observed after GM injections only in Group II. Even in the 11 patients who showed an improvement in hearing of more than 10 dB (hearing improvement group), percentage of canal paresis was increased after GM. More, premedication plasma vasopressin levels were lower in the hearing improvement group as compared with the hearing loss/no changes group. Four of eight patients became negative for dominant negative summating potential in electrocochleography after GM injections in the hearing improvement group. Our data indicate that the frequency of vertigo is not a key factor in the vertigo control after GM injections, that induction of vestibular damage in the injected ear is essential for the control of vertigo and this effect is mostly pronounced in patients with milder hearing loss, and that hearing improvement is not only a consequence of good vertigo control but also affected by the stress level before treatment.

Lesion of the anteroventral third ventricle (AV3V) reduces hypothalamic activation and hypophyseal hormone secretion induced by lipopolysaccharide in rats

This study examined whether electrolytic ablation of the periventricular anteroventral third ventricle (AV3V) region would affect the hypothalamic activation and the increase of hypophysial hormone secretion induced by systemic injection of lipopolysaccharide (LPS) in rats. LPS significantly increased the number of cells showing Fos immunoreactivity in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus ( P < 0.05) and also increased plasma levels of vasopressin, oxytocin, adrenocorticotropin and corticosterone ( P < 0.05). AV3V lesion significantly reduced LPS-induced Fos immunoreactivity ( P < 0.05) and vasopressin and oxytocin secretion ( P < 0.05). Elevations in adrenocorticotropin but not in plasma corticosterone after LPS were affected by prior AV3V lesions. These findings demonstrate that LPS-induced Fos expression in the PVN and SON, and hypophysial hormone secretion is dependent on the integrity of the AV3V region.

Antidiuretic Hormone and Osmolality in Isosorbide Therapy and Glycerol Test

Changes in plasma antidiuretic hormone (p-ADH) and plasma osmolality (p-Osm) levels were studied in 63 patients with Ménière’s disease before and after isosorbide administration and a glycerol test. Increments in both p-ADH and p-Osm levels were observed after isosorbide administration and the glycerol test. The p-ADH secretion appeared to be secondarily stimulated by an increase in the p-Osm level. This p-ADH level increase affects cochlear fluid homeostasis. Based on these results, we must consider both the p-Osm and p-ADH levels when treating patients with Ménière’s disease by osmotic diuretics.

Participation of the subfornical nucleus in hypothalamic-neurohypophyseal axis activation during the early phase of endotoxic shock

During the early phase of endotoxic shock the hypothalamus is activated and neurohypophyseal hormone secretion is increased. In order to study the participation of the subfornical organ (SFO) in this response we lesioned the nucleus and determined hormone secretion and c- fos expression in the paraventricular and supraoptic nuclei after administration of lipopolysaccharides (LPS) in rats. LPS significantly increased the number of cells showing Fos immunoreactivity in the paraventricular and supraoptic nuclei of the hypothalamus ( p < 0.05) and also caused an increase in plasma levels of vasopressin and oxytocin ( p < 0.05). SFO lesion significantly reduced LPS-induced Fos immunoreactivity ( p < 0.05) and hormone secretion ( p < 0.05). We conclude that the SFO participates in the activation of the hypothalamic-neurohypophyseal axis in the early phase of endotoxic shock.

Intravenous 6-hydroxydopamine attenuates vasopressin and oxytocin secretion stimulated by hemorrhage and hypotension but not hyperosmolality in rats

The present study sought to determine whether chemical destruction of peripheral catecholaminergic fibers with 6-hydroxydopamine (6OHDA) attenuates vasopressin (VP) and oxytocin (OT) secretion stimulated by hemorrhage, hypotension, and hyperosmolality. Rats received 6OHDA (100 mg/kg iv) or vehicle (1 ml/kg iv) on days 1 and 7, and experiments were performed on day 8. Serial hemorrhage (4 samples of 2 ml per 300 g body wt at 10-min intervals) increased plasma VP and OT levels in both groups; however, the increase in plasma VP and OT levels was significantly attenuated in 6OHDA-treated vs. control rats despite a significantly lower mean arterial blood pressure. Similarly, the increase in plasma VP and OT levels in response to hypotension produced by the selective arteriolar vasodilator diazoxide was significantly attenuated in 6OHDA-treated rats. In marked contrast to hemorrhage and hypotension, hyperosmolality produced by an infusion of 1 M NaCl (2 ml/h iv) stimulated increases in plasma VP and OT levels that were not different between 6OHDA-treated and control rats. In a parallel set of experiments, intravenous 6OHDA treatment reduced dopamine--hydroxylase immunoreactivity in the posterior pituitary but had no substantial effect in the hypothalamic paraventricular and supraoptic nuclei. In each experiment, the pressor response to tyramine (250 microg/kg iv) was significantly attenuated in 6OHDA-treated rats, thereby confirming that 6OHDA treatment destroyed sympathetic catecholaminergic fibers. Collectively, these findings suggest that catecholaminergic fibers located outside the blood-brain barrier contribute to VP and OT secretion during hemorrhage and arterial hypotension.

A Rare Case of Combined Syndrome of Inappropriate Antidiuretic Hormone Secretion and Fanconi Syndrome in an Elderly Woman

An 83-year-old Japanese woman was admitted to our hospital with severe hyponatremia (sodium, 108 mEq/L [108 mmol/L]), hypokalemia, hypochloridemia, hypocalcemia, hypophosphatemia, and hypouricemia. Despite low plasma osmolarity (232 mOsm/kg [232 mmol/kg]), urine osmolarity (320 mOsm/kg) was greater than that of plasma, and she had increased urinary sodium excretion (88 mEq/L [88 mmol/L]) and an unsuppressed high plasma level of antidiuretic hormone (ADH; 5.5 pg/mL [5.1 pmol/L]). These findings indicated that she had syndrome of inappropriate ADH secretion (SIADH). In addition, she had a generalized reabsorption defect of the proximal tubules, including decreased tubular reabsorption of phosphate, increased fractional excretion of uric acid, glycosuria despite a normal blood glucose level, and panaminoaciduria. Thus, combined SIADH and Fanconi syndrome was diagnosed. The cause was thought to be the antidepressant paroxetine, which is a selective serotonin reuptake inhibitor (SSRI). Several of the abnormal values resolved within 1 week after discontinuation of this drug. Although the precise mechanism responsible was not elucidated, we report an extremely rare case of combined SIADH and Fanconi syndrome, probably caused by short-term SSRI therapy.

Effects of i.c.v. losartan on the angiotensin II-mediated vasopressin release and hypothalamic fos expression in near-term ovine fetuses

Our previous studies have shown that central administration of angiotensin (ANG II) causes arginine vasopressin (AVP) release in the fetus at 70–90% gestation. This is evidence that the hypothalamic-neurohypophysial system is relatively mature before birth. However, few data exist regarding central ANG receptor mechanisms-mediated AVP response during fetal life. To determine roles of brain ANG receptor subtypes in this response, AT 1 and AT 2 receptor antagonists, losartan and PD123319, were investigated in the brain in chronically prepared ovine fetuses at the last third of gestation. Application of losartan intracerebroventricularly (i.c.v.) at 0.5 mg/kg suppressed central ANG II-stimulated plasma AVP release. Losartan at 5 mg/kg (i.c.v.) demonstrated a significant enhancement of AVP increase to i.c.v. ANG II. Associated with the increase of plasma vasopressin levels, c-fos expression in the hypothalamic neurons was significantly different between the low and high doses of losartan. The low dose losartan markedly reduced the dual immunoreactivity for FOS and AVP in the supraoptic nuclei and paraventricular nuclei after i.c.v. ANG II, whereas the high dose losartan together with ANG II, significantly increased the co-localization of positive FOS in the AVP-containing neurons than that induced by i.c.v. ANG II alone. Central ANG II induced fetal plasma vasopressin increase was not altered by PD123319. The data suggest that losartan in the fetal brain has remarkably different effects based on the doses administrated on central ANG II-related neuroendocrine effects at the late gestation, and that the AT 1 mechanism is critical in the regulation of fetal body fluid homeostasis related to plasma AVP levels.

Attenuation of homeostatic responses to hypotension and glucoprivation after destruction of catecholaminergic rostral ventrolateral medulla neurons

This study determined the effect of destruction of rostral ventrolateral medulla (RVLM)-C1 cells on integrated sympathetic and hormonal responses to hypotension or glucoprivation. Injection of anti-dopamine beta-hydroxylase-saporin into the RVLM resulted in 29-99% depletion of RVLM-C1 neurons and approximately 60% reduction in the number of A5 neurons. As in our previous study in unanesthetized rats, resting mean arterial pressure (MAP) was reduced by approximately 10 mmHg in rats with >80% depletion of RVLM-C1 cells compared with control rats, although resting heart rate (HR) did not differ significantly. In the present study, resting plasma levels of norepinephrine (NE) did not differ significantly between control rats and rats with >80% depletion of RVLM-C1 cells, although there was a tendency for RVLM-C1 lesioned rats to have lower levels. Also consistent with our previous study, hydralazine (HDZ)-evoked hypotension resulted in smaller increases in HR and plasma levels of NE in rats with >80% depletion of RVLM-C1 cells compared with control rats. Furthermore, the elevated plasma levels of posterior pituitary hormones vasopressin and oxytocin evoked by HDZ were blunted in RVLM-C1 lesioned rats compared with control rats, even though MAP fell to lower levels in the lesioned rats. Plasma renin activity, plasma osmolality, and plasma protein concentrations did not differ between control rats and rats with >80% depletion of RVLM-C1 neurons. In response to systemic administration of 2-deoxyglucose, the circulating level of epinephrine and the resulting hyperglycemia were attenuated in rats with >80% depletion of RVLM-C1 cells compared with control rats. These results demonstrate that RVLM-C1 cells, in addition to playing a role in acute cardiovascular reflexes, play an important role in integrated sympathetic and hormonal responses to homeostatic challenges such as hypotension and glucoprivation.

Hyponatremia Impairs Early Posttransplantation Outcome in Patients With Cirrhosis Undergoing Liver Transplantation

Hyponatremia is associated with reduced survival in patients with cirrhosis awaiting liver transplantation. However, it is not known whether hyponatremia also represents a risk factor of poor outcome after transplantation. We aimed to assess the effects of hyponatremia at the time of transplantation on posttransplantation outcome in patients with cirrhosis. Two-hundred forty-one consecutive patients with cirrhosis submitted to liver transplantation during a 4-year period (January 2000-December 2003) were included in the study. The main end point was survival at 3 months after transplantation. Secondary end points were complications within the first month after transplantation. Patients with hyponatremia (serum sodium lower than 130 mEq/L) had a greater incidence of neurologic disorders, renal failure, and infectious complications than patients without hyponatremia (odds ratio; 4.6, 3.4 and 2.7, respectively) within the first month after transplantation. By contrast, hyponatremia was not associated with an increased incidence of severe intra-abdominal bleeding, acute rejection, or vascular and biliary complications. Hyponatremia was an independent predictive factor of early posttransplantation survival. Three-month survival of patients with hyponatremia was 84% compared with 95% of patients without hyponatremia (P < .05). Survival was similar after 3 months. In patients with cirrhosis, the presence of hyponatremia is associated with a high rate of neurologic disorders, infectious complications, and renal failure during the first month after transplantation and reduced 3-month survival. In cirrhosis, hyponatremia should be considered not only a risk factor of death before transplantation but also a risk factor of impaired early posttransplantation outcome.

Hypertonic NaCl infusions affect milk composition in goats

The capability of goats to maintain milk production during water deprivation is remarkable and not yet fully understood. The aim of the present study was to investigate whether intravenous infusions of hypertonic NaCl cause release of both vasopressin and oxytocin and whether the peptides, in combination with the hyperosmolality, affect milk flow and milk composition. Six Swedish domestic landrace goats in their first to third lactation were milked every 30 min during experiments. Hypertonic NaCl (HNaCl) or isotonic NaCl (IsoNaCl) were infused for 90 min. Goats were not allowed to drink during infusions. Plasma vasopressin concentration increased during HNaCl infusions, and did not change in response to IsoNaCl infusions. Plasma oxytocin concentration did not change during either infusion. Milk flow was maintained during the infusions. Milk fat concentration decreased in the three samples taken before onset of the infusions, but then increased gradually during HNaCl infusions, while it continued to fall during the IsoNaCl infusions. Milk osmolality followed the rise in plasma osmolality during the HNaCl infusions and did not change in IsoNaCl experiments. Milk lactose concentration increased throughout both series of experiments, the concentration being higher during HNaCl infusions. Milk protein concentration did not change during HNaCl infusions, but fell in the IsoNaCl experiments. It is concluded that the hyperosmolality in combination with elevated plasma vasopressin levels did not disturb the secretory activity of the mammary cells, but rather facilitated emptying of the alveolar milk. Such a mechanism may help to explain the sustained milk production in water deprived goats.

Vasopressin and nitric oxide synthesis after three days of water or food deprivation

Nitric oxide has been suggested to be involved in the regulation of fluid and nutrient homeostasis. In the present investigation, vasopressin and nitric oxide metabolite (nitrite and nitrate) levels were determined in plasma of male Wistar rats submitted to water or food deprivation for three days. Hematocrit and plasma sodium showed marked increase in dehydrated and starved rats. Potassium levels and plasma volume decreased in both treated groups. Plasma osmolality and vasopressin levels were significantly elevated in water deprived (362.8 +/- 7.1 mOsm/kg H2O, 17.3 +/- 2.7 pg/ml, respectively, p < 0.001) rats, but not in food deprived (339.9 +/- 5.0, 1.34 +/- 0.28) rats, compared to the controls (326.1 +/- 4.1, 1.47 +/- 0.32). The alterations observed in plasma vasopressin levels were related to plasma osmolality rather than plasma volume. Plasma levels of nitrite and nitrate were markedly increased in both water and food deprived rats (respectively, 2.19 +/- 0.29 mg/l and 2.22 +/- 0.17 mg/l versus 1.33 +/- 0.19 mg/l, both p < 0.01). There was a significant negative correlation between plasma nitrite and nitrate concentration and plasma volume. These results suggest that both dehydration and starvation increase plasma nitric oxide, probably by activation of nitric oxide synthases. The release of nitric oxide may participate in the regulation of the alteration in blood flow, fluid and nutrient metabolism caused by water deprivation or starvation.

Increased Arginine Vasopressin mRNA Expression in the Human Hypothalamus in Depression: A Preliminary Report

Elevated arginine vasopressin (AVP) plasma levels have been observed in major depression, particularly in relation to the melancholic subtype. Two hypothalamic structures produce plasma vasopressin: the supraoptic nucleus (SON) and the paraventricular nucleus (PVN). The aim of this study was to establish which structure is responsible for the increased vasopressin plasma levels in depression. Using in situ hybridization, we determined the amount of vasopressin messenger ribonucleic acid (mRNA) in the PVN and SON in postmortem brain tissue of nine depressed subjects (six with the melancholic subtype) and eight control subjects. In the SON, a 60% increase of vasopressin mRNA expression was found in depressed compared with control subjects. In the melancholic subgroup, AVP mRNA expression was significantly increased in both the SON and the PVN compared with control subjects. We found increased AVP gene expression in the SON in depressed subjects. This might partly explain the observed increased vasopressin levels in depression.

Depression with above-normal plasma vasopressin: Validation by relations with family history of depression and mixed anxiety and retardation

An anxious-retarded subtype of depression has been derived from the DSM-IV category of melancholia. It is defined by combined high scores for anxiety and retardation, and is related to family history of depression and increased plasma vasopressin (AVP) levels. Central problems concerning this hypothesized subcategory are whether elevated plasma AVP is related to family history, whether it would be better operationalized by a cut-off level for plasma AVP than as continuous variable, and whether the anxious-retarded phenotype would be better described in terms that account for full variability of mixed anxiety and retardation. A previous study suggested that above-normal plasma AVP was a more useful endophenotypic parameter than plasma AVP as a continuous variable. To answer these and related questions, 81 patients were investigated. Receiver Operating Characteristic analyses yielded a cut-off value of 5.56 pg/ml for above-normal plasma AVP, log-transformed plasma AVP (ln (AVP)) was used as continuous variable, and the correlation between anxiety and retardation was used to account for full variability of the anxious-retarded phenotype. Family history was related to above-normal plasma AVP ( n = 16) and non-significantly to ln (AVP). Depression with above-normal plasma AVP, as well as familial depression with above-normal plasma AVP, showed a high correlation between anxiety and retardation, and this correlation was significantly higher than that found in the depressed patient control groups. The data support the delimitation of a largely familial depression with above-normal plasma AVP, vasopressinergic activation of the hypothalamus–pituitary–adrenal axis and a variable anxious-retarded phenotype.

Increased Expression of Renal Aquaporin Water Channels in Spontaneously Hypertensive Rats

Aims: The present study was aimed to determine whether there exists an altered regulation of aquaporin (AQP) water channels in hypertension. Methods: Male spontaneously hypertensive rats (SHR) aged 10–12 weeks were used. Age-matched Wistar-Kyoto (WKY) rats served as control. The abundance of AQP1–4 proteins in the kidney was determined by Western blot analysis. The protein expression and activity of adenylyl cyclase were also determined. Results: The medullary expression of AQP2 and AQP3 proteins was increased in SHR compared with that in WKY rats. The expression of AQP1 protein was also significantly increased in the inner medulla, while that of AQP4 was not. Immunohistochemistry of AQP2 revealed that principal cells of the collecting duct have strong immunoreactivity, the degree of which was augmented with prominent apical labeling in SHR. The plasma level of arginine vasopressin (AVP) was higher in SHR; the adenylyl cyclase activity stimulated by AVP was augmented, along with increased expression of type VI adenylyl cyclase. The urine was more concentrated with its volume decreased in SHR. Conclusion: The expression of AQP1–3 channels is increased in the kidney, in association with enhanced activity of the AVP/cAMP pathway, in SHR.

Agonist and hypertonic saline-induced trafficking of the NK3-receptors on vasopressin neurons within the paraventricular nucleus of the hypothalamus

The neurokinin 3 receptor (NK3R) is colocalized with vasopressinergic neurons within the hypothalamic paraventricular nucleus (PVN) and intraventricular injections of NK3R agonists stimulate vasopressin (VP) release. Our objectives were to test the hypotheses that intraventricular injections of the selective NK3R agonist, succinyl-[Asp6, N-Me-Phe8] substance P (senktide), activate NK3R expressed by vasopressinergic neurons within the PVN, and see whether NK3R expressed by vasopressinergic neurons in the PVN are activated by hyperosmolarity. NK3R internalization was used as a marker of receptor activation. Immunohistochemistry revealed that NK3Rs were membrane-bound on VP immunoreactive neurons in control rats. Following senktide injection, there was a significant increase in the appearance of NK3R immunoreactivity within the cytoplasm and a morphological rearrangement of the dendrites, indicating receptor internalization, which was reversible. Furthermore, pretreatment with a selective NK3R antagonist, SB-222200, blocked the senktide-induced VP release and internalization of the NK3R in the PVN. These results show that the trafficking of the NK3R is due to ligand binding the NK3R. In a subsequent experiment, rats were administered intragastric loads of 2 or 0.15 M NaCl, and NK3R immunohistochemistry was used to track activation of the receptor. In contrast to control rats, 2 M NaCl significantly increased plasma VP levels and caused the internalization of the NK3R on VP neurons. Also, NK3R immunoreactivity was located in the nuclei of vasopressinergic neurons after senktide and 2 M NaCl treatment. These results show that hyperosmolarity stimulates the local release of an endogenous ligand in the PVN to bind to and activate NK3R on vasopressinergic neurons.

Stimulus for vasopressin release during elective intra-abdominal operations.

In 12 patients undergoing an upper abdominal operation, blood pressure and peripheral venous blood samples were taken at intervals throughout the procedure. There was no significant increase in plasma vasopressin concentration after induction of anaesthesia or skin incision; within 3 min of opening the peritoneum and commencing intraperitoneal manipulation there was a highly significant rise (P less than 0.01), maintained with fluctuations until closure of the abdomen. There was no correlation between the changes of blood pressure and those in plasma vasopressin level. In 16 patients undergoing elective cholecystectomy similar observations were made to coincide with events believed, on the basis of the first study, to be related to changes in the concentration of vasopressin. There was a significant rise in vasopressin concentration (P less than 0.01) after incision of the peritoneum, 1 min after the start of intraperitoneal manipulation (P less than 0.01) and after deliberate traction on the stomach (P less than 0.01). During operative cholangiography, when there was no intraperitoneal manipulation, there was a significant fall in the vasopressin level. There was no correlation between changes in vasopressin concentration and blood pressure. These findings indicate that during an abdominal operation nervous stimuli, arising from within the peritoneal cavity and probably mediated via the autonomic system, are an important factor responsible for the increased secretion of vasopressin, and, at least in the absence of major changes in blood pressure and osmolality, the determinant factor.

Vasopressin effects on the small intestine: a possible factor in paralytic ileus?

Experiments were performed on luminally perfused, isolated, canine, jejunal segments in vivo to determine the effects of vasopressin on intestinal motility, myoelectrical activity and absorption. Intravenous vasopressin abolished spike activity and sometimes disrupted slow wave activity. The jejunum became atonic with intraluminal pooling of perfusate. Transit time was prolonged and intestinal absorption of water was decreased. Radionuclide imaging of the intestinal contents showed a doubling of intraluminal volume with vasopressin and confirmed the loss of intestinal motility. It is suggested that the high plasma levels of vasopressin which are known to follow laparotomy may be a factor in the development of postoperative ileus.

Anxious-retarded depression: Relation to two-year outcome of major depressive disorder

Background Anxious-retarded depression is a two-dimensionally defined subcategory of depression derived from DSM-IV melancholia. It is related to increased plasma vasopressin, correlative plasma vasopressin and cortisol levels, and a positive family history. We now explored its relation with outcome. Methods Seventy depressed patients were included to follow-up for two years. Outcome was defined by time until full-remission. Cox regression analyses were used to compare anxious-retarded and non-anxious-retarded patients, as well as melancholic and non-melancholic patients. Results Anxious-retarded depression had poor outcome. Limitations The number of patients was relatively small. Conclusion The poor outcome of anxious-retarded depression further supports its validity.

The association of antidiuretic hormone levels with an attack of Meniere's disease

An elevation of the plasma antidiuretic hormone (ADH) levels has frequently been observed in Meniere's disease patients. However, little is known regarding the mechanism behind such an elevation of ADH level in Meniere's disease patients. Therefore, we measured the plasma ADH in Meniere's disease patients and other vertigo patients to elucidate the association between the ADH levels, stress levels and the development of Meniere's symptom. The plasma ADH levels and plasma osmotic pressure were determined in 23 definite Meniere's disease patients and 160 patients with other types of vertigo/dizziness. All participants were administered questionnaire regarding their psychological status including their stress levels. The ADH levels of Meniere's disease patients in the acute phase (5.80 +/- 1.37 pg/mL) were significantly higher in comparison with that of Meniere's disease patients in the remission phase (2.26 +/- 0.41 pg/mL) (P < 0.05). In other peripheral vertigo patients, the ADH level in the acute phase (1.71 +/- 0.23 pg/mL) was not significantly different from that in the remission phase (1.45 +/- 0.15 pg/mL). Meniere's disease patients in the acute phase had a significantly higher stress score (114 +/- 23) than Meniere's disease patients in the remission phase (56 +/- 13) (P < 0.05). However, there was no significant correlation between their stress score and the ADH levels. These results suggest that the elevation of the plasma ADH levels in Meniere's disease patients in the acute phase is, therefore, associated with the pathogenesis of Meniere's disease attacks rather than with stress.

Plasma Vasopressin, an Etiologic Factor of Motion Sickness in Rat and Human?

Arginine vasopressin (AVP) is considered as an etiologic hormone in motion sickness. However, the possible role of plasma AVP in motion sickness is still controversial. A number of studies have found a gender difference in susceptibility to motion sickness in humans and experimental animals, with female subjects being more susceptible. However, the existence of a gender difference in the AVP response to motion sickness is not known. This study was designed to verify the assumption that plasma vasopressin plays a role in motion sickness.Changes in plasma vasopressin were observed after motion sickness-inducing rotatory stimuli in both sexes in human subjects and rats receiving or not antimotion sickness treatments. Plasma vasopressin levels in motion sickness rats exhibited a decrease after rotation in female, but not in male rats. The vasopressin content of the pituitary increased in both sexes. Plasma vasopressin in rats of both sexes tended to increase after a 15-day adaptive training of rotation, but pituitary vasopressin content was not affected under this condition. In contrast, in human subjects, plasma vasopressin levels increased after rotation in all males, but not in females. When antimotion sickness drugs (domperidone 10 mg + flunarizine 5 mg) were administered, plasma vasopressin levels were elevated in both females and males. It is concluded that plasma vasopressin increases after motion sickness-induced stimulation provided subjects have become trained to motion sickness. These results do not support an etiologic role of plasma vasopressin in the genesis of motion sickness.