Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The stress of motion sickness was experimentally provoked by Coriolis effect. Significant and reproducible increases from the basal serum level (delta mean +/- S.E.) of antidiuretic hormone delta - ADH: 48.2 +/- 4.6 pg/ml; p less than 0.0005), of growth hormone (delta - hGH: 10.0 +/- 1.2 ng/ml; p less than 0.0005), of prolactin (delta - hPRL: 186.5 +/- 29.9 muU/ml; p less than 0.0005), and of cortisol (delta - F; 12.3 +/- 0.9 microgram%; p less than 0.0005) were observed, whereas the luteinizing hormone levels did not change significantly. The stimulation of hormone secretion induced by different degrees of motion sickness seems to correlate with the severity of motion sickness. The secretion of antidiuretic hormones is the most sensitive indicator for the stress of motion sickness whereas growth hormone, prolactin, and cortisol responses to the stress of motion sickness are more delayed and less pronounced.
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PMID:Increased secretion of growth hormone, prolactin, antidiuretic hormone, and cortisol induced by the stress of motion sickness. 62 65

Fundamental approaches in selection of new agents for evaluation in prevention of space/motion sickness (SMS) are reviewed. The discussion centers on drugs under investigation at the Johnson Space Center. Methodology that employs the rotating chair for measuring SMS symptomatology and susceptibility is described. The most obvious approach to the development of new agents relies on selection of agents from drug classes that possess pharmacologic properties of established anti-motion sickness agents. A second approach selects drugs that are used to prevent emesis caused by means other than exposure to motion. The third approach relies on basic research that characterizes individual differences in susceptibility. The hypothesis is: detection of individual differences leads to identification of specific drugs, which target physiologic systems that show individual differences. These physiologic systems are targets for therapy and may play a role in the etiology of SMS. Two drugs that reduce susceptibility to SMS include dexamethasone and d(CH2)5Tyr(Me)AVP, a vasopressin (AVP)V1 antagonist. The latter peptide has demonstrated complete blockade of emesis and other significant symptoms in squirrel monkeys. These studies were predicated on observations that subjects who were more resistant to SMS had higher plasma AVP after severe nausea than subjects with lower resistances. Investigations are underway to test a 0.5-mg intravenous dose in humans. Kappa opioid agonists inhibit AVP release and offer new therapeutic possibilities and advantages over AVP peptides. This review details the experimental data collected on AVP and adrenocorticotropin. The literature supports interrelated roles for AVP and opioid peptides in SMS. Experimental testing of kappa agonists is warranted because specific opioid agonists act at neuroanatomical sites causing nausea and vomiting. It is argued opioid receptors in the chemoreceptor trigger zone and vomiting center stimulate and inhibit the emetic response, respectively. The evidence suggests kappa and/or mu receptors at VC are involved in inhibition of emesis, whereas delta opioid receptors at CTZ are involved in stimulation of emesis.
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PMID:New pharmacologic approaches to the prevention of space/motion sickness. 166 31

The physiology of nausea, a uniquely human symptom, is poorly understood. The purpose of this study was to measure the temporal sequences of neurohormonal responses and gastric myoelectrical activity in healthy subjects during the rotation of an optokinetic drum that produced nausea and other symptoms of motion sickness. Plasma catecholamines, vasopressin, and cortisol were measured at baseline, during minutes 1-5, 6-10, and 11-15 of drum rotation, and after rotation stopped. Electrogastrograms were recorded throughout the study. Twelve subjects (80%) developed nausea and 4-9 cycles/min of gastric tachyarrhythmias; three subjects had no nausea and no gastric dysrhythmias. Tachyarrhythmias began 3.4 +/- 0.8 min after the onset of drum rotation, and nausea was reported, on average, 3 min later. During minutes 6-10 of drum rotation, vasopressin levels significantly increased in the subjects with nausea compared with subjects without nausea (P < 0.04). In the subjects with nausea, epinephrine and vasopressin increased significantly (P < 0.05) compared with baseline during minutes 6-10 and 11-15 of drum rotation. As nausea resolved during recovery, vasopressin decreased by 74%, whereas epinephrine increased 13%. We conclude that 1) in nauseated subjects, endogenous vasopressinergic and sympathetic circuits are activated before hypothalamic-pituitary-adrenal pathways, 2) plasma vasopressin levels correlate most closely with the temporal onset and resolution of nausea, and 3) peripheral gastric dysrhythmias may have a role in activating central vasopressinergic neurons.
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PMID:Hypothalamic and gastric myoelectrical responses during vection-induced nausea in healthy Chinese subjects. 823 33

A rotating optokinetic drum was used in three laboratory studies to test the hypothesis that Asian subjects are hypersusceptible to motion sickness. The results of the first study showed that Chinese women compared to European-American and African-American women experienced significantly more severe symptoms of motion sickness and greater disturbance of normal gastric myoelectric activity. A second study yielded similar results using American-born children of Asian parents. The results of a third study using Chinese men and women were similar and showed a significant increase in vasopressin during rotation. Possible genetic mechanisms that may account for these results are discussed.
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PMID:Asian hypersusceptibility to motion sickness. 882 56

The possible role of vasopressin in nausea and gastric dysrhythmias in motion sickness was tested by electrogastrography in 14 subjects during circular vection (60 degrees/s) and vasopressin infusion. Tachygastria was expressed as the signal percent >4.5 cycles/min. Vection evoked nausea scores of 2.6 +/- 0.2 (0 = none to 3 = severe) in 10 subjects with increases in tachygastric activity (15 +/- 2 to 45 +/- 3%) and plasma vasopressin (4.5 +/- 1.5 to 8.4 +/- 2.5 pg/ml) that were blocked by atropine but not indomethacin. Four asymptomatic subjects had no tachygastria or vasopressin release. Vasopressin at 0.2 U/min (plasma level = 322.1 +/- 10.3 pg/ml) evoked nausea (2.6 +/- 0.4) and increases in tachyarrhythmic activity (41 +/- 5%) that were blunted by atropine but not indomethacin. There were no differences in nausea or dysrhythmias with vasopressin infusion in subjects who noted nausea during vection versus those who did not. To conclude, vection evokes nausea, dysrhythmias, and vasopressin release in motion sickness-susceptible humans via cholinergic prostaglandin-independent pathways. Supraphysiological vasopressin infusions evoke nausea and dysrhythmias by similar pathways to equal degrees in motion sickness-susceptible and -resistant subjects. Thus central but not peripheral actions of vasopressin may contribute to nausea and slow wave disruption with vection. Blunting of both the release and action of vasopressin by atropine may explain its beneficial action in motion sickness.
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PMID:Role of plasma vasopressin as a mediator of nausea and gastric slow wave dysrhythmias in motion sickness. 914 18

Motion sickness provides a unique setting for the study of nausea. Studies of illusory self-motion have linked nausea and objective measures of gastric dysrhythmias and the stress hormones vasopressin and epinephrine. Electrogastrographic methods utilize Ag-AgCl electrodes placed on the abdominal surface in the epigastric region to record electrogastrograms (EGGs), a noninvasive measure of gastric myoelectrical activity. The EGG frequencies of interest are the normal range (2.4-3.6 cpm), tachygastrias (3.6-9.9 cpm), and bradygastrias (1.0-2.4 cpm), and duodenal respiratory frequencies (10.0-15.0 cpm). Illusory self-motion or vection is produced with a rotating drum. Minutes before vection-induced nausea is reported, the baseline EGG signal shifts into tachygastrias or mixed tachygastrias and bradygastrias. Quantitative analyses show that the percentage of power in the tachygastria range correlates with the intensity of nausea. Plasma vasopressin levels correlate positively with intensity of nausea. Asian subjects have higher intensity nausea and higher vasopressin levels compared with Caucasian subjects, indicating a potential genetic susceptibility to vection-induced motion sickness and nausea. Vection-induced motion sickness represents an experimental model of acute-onset nausea with accompanying symptoms such as headache, drowsiness, cold sweating, and fatigue. Illusory self-motion is a purely central nervous system (visual-vestibular) stimulation that evokes dramatic shifts in gastric electrical activity and significant release of the posterior pituitary hormone vasopressin. Central nervous systems pathways that evoke gastric dysrhythmias and release vasopressin may also have a pathophysiologic role in the cyclic vomiting syndrome.
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PMID:Illusory self-motion and motion sickness: a model for brain-gut interactions and nausea. 1049 40

Duodenal lipid causes gastric relaxation, CCK secretion, and nausea. Vasopressin has been implicated in motion sickness-related nausea. We hypothesized that increasing doses of lipid enhance gastric relaxation and CCK-vasopressin secretion, resulting in a dose-related exacerbation of nausea. Nine healthy subjects received isotonic saline or lipid (1, 2, or 3 kcal/min, L1, L2, L3) duodenally. Changes in gastric volume, sensations, and plasma hormone levels were assessed during infusions and isobaric gastric distensions. Lipid infusions increased gastric volume, plasma CCK (but not vasopressin) levels, and gastric compliance during distensions, compared with saline. Plasma CCK levels were related to the dose of lipid administered [CCK levels at 30 min (pmol/l), saline: 1.1 +/- 0.2, L1: 1.8 +/- 0.2, L2: 3.0 +/- 0.2, L3: 4.3 +/- 0.6]. During distensions, nausea increased in intensity with increasing doses of lipid [score (where 0 is no sensation and 100 is strongest sensation), saline: 7 +/- 4, L1: 19 +/- 7, L2: 44 +/- 7, L3: 66 +/- 8]; however, no further rise in plasma CCK occurred. Because neither lipid nor distension alone induced significant nausea, we conclude that the interaction between these stimuli together with a modulation by CCK is responsible for the effects observed. Vasopressin is not involved in lipid- and distension-induced nausea.
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PMID:Relationship between increasing duodenal lipid doses, gastric perception, and plasma hormone levels in humans. 1080 Dec 90

Recent studies, which have shown an increase of plasma vasopressin (VP) in experimental motion sickness and the efficacy of VP antagonists for motion sickness, suggest an important role of VP in the development of vestibulo-autonomic responses. We have recently found evidence of the co-existence of vasopressinergic neurons with the stress-sensitive chemokinergic neuronal system in the hypothalamo-pituitary pathway in rats, which uses cytokine-induced neutrophil chemoattractant (CINC) as an effector molecule. In this study, to elucidate possible roles of VP and CINC in the vestibulo-autonomic responses, we simultaneously measured plasma VP and CINC concentrations after electrical or caloric vestibular stimulation in urethane-anesthetized rats. Electrical vestibular stimulation with more than 200 microA increased the plasma levels of VP in a current intensity-dependent manner, and stimulation with 500 microA increased the plasma VP levels to 350% of the normal control group, which received no stimulation. Caloric vestibular stimulation with cold water increased the plasma VP levels to 262% of the control group, which received caloric stimulation with water at 37 degrees C, and stimulation with warm water tended to increase the plasma VP levels. Plasma CINC levels were neither affected by electrical nor caloric vestibular stimulation. These findings indicate that vestibular stimulation increased plasma levels of VP but not CINC, and this vestibular-induced activation of VP neurons may be involved in a mechanism of vestibulo-autonomic responses.
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PMID:Vestibular modulation of plasma vasopressin levels in rats. 1157 10

Space flight exerts substantial effects on fluid volume control in humans. Cardiac distension occurs during the first 1-2 days of space flight relative to supine and especially upright 1g conditions. Plasma volume contraction occurs quickly in microgravity, probably as a result of transcapillary fluid filtration into upper-body interstitial spaces. No natriuresis or diuresis has been observed in microgravity, such that diuresis cannot explain microgravity-induced hypovolemia. Reduction of fluid intake occurs irrespective of space motion sickness and leads to hypovolemia. The fourfold elevation of urinary antidiuretic hormone (ADH) levels on flight day 1 probably results from acceleration exposures and other stresses of launch. Nevertheless, it is fascinating that elevated ADH levels and reduced fluid intake occur simultaneously early in flight. Extracellular fluid volume decreases by 10-15% in microgravity, and intracellular fluid volume appears to increase. Total red blood cell mass decreases by approximately 10% within 1 week in space. Inflight Na(+) and volume excretory responses to saline infusion are approximately half those seen in pre-flight supine conditions. Fluid volume acclimation to microgravity sets the central circulation to homeostatic conditions similar to those found in an upright sitting posture on Earth. Fluid loss in space contributes to reduced exercise performance upon return to 1g, although not necessarily in flight. In-flight exercise training may help prevent microgravity-induced losses of fluid and, therefore, preserve the capacity for upright exercise post-flight. Protection of orthostatic tolerance during space flight probably requires stimulation of orthostatic blood pressure control systems in addition to fluid maintenance or replacement.
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PMID:Fluid volume control during short-term space flight and implications for human performance. 1158 36

The possibility that drugs administered to Skylab 3 (SL-3) and 4 (SL-4) crewmen for space motion sickness may have interfered with their biomedical evaluation in space was investigated. Healthy volunteers received combinations of Scopolamine/Dexedrine for four days in regimens similar to those used in these missions. Urine samples, heart rate, body temperature, mood and performance were analyzed for drug-related changes. Twenty-four hour urine samples were analyzed by the same procedures as those used to analyze the flight samples. Hormone concentrations determined included cortisol, epinephrine, norepinephrine, aldosterone and antidiuretic hormone (ADH). In addition, volume, specific gravity, osmolarity, sodium (Na), potassium (K), calcium (Ca), magnesium (Mg), chloride (Cl), inorganic phosphate, uric acid and creatinine were measured. Performance was not affected by the Scopolamine/Dexedrine. The drug combination increased daily mean heart rate (HR) significantly in all the subjects and daily mean rectal temperature (RT) in some of the subjects. A 2-4 hr phase shift in the HR circadian rhythm was also observed which indicates that internal circadian synchrony was disturbed by the drugs. Psychological and subjective evaluation indicated that the subjects could usually identify which days they were given the drugs by an increase in tension and anxiety, decreased patience, restlessness, decreased appetite, difficulty in sleeping and feelings of increased heart rate and body temperature. Urinary electrolytes were not changed significantly by the drug, but marked and significant changes occurred in urine volume and hormone excretion patterns. Scopolamine/Dexedrine caused consistent elevations in urinary cortisol and epinephrine and a transient elevation in ADH. Norepinephrine excretion was decreased, but there was no significant change in aldosterone excretion or in 24 hr urine volume. A comparison of these findings with the first four days of inflight data from the SL-3 and SL-4 missions leads to the conclusion that the dramatic increases in aldosterone excretion during the first three days of spaceflight probably can be directly attributed to weightlessness, whereas the antimotion sickness medication could have substantially contributed to the early increased excretion of epinephrine and cortisol during these missions.
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PMID:Space motion sickness medications: interference with biomedical parameters. 1182 24


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