Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin (AVP) secretion is principally under osmotic regulation, which is altered by nonosmotic stimuli. It is known that the manner of osmotic regulation of AVP secretion in hypoosmolar state of man consists of four types. The types have (A) random changes in plasma AVP without relation of plasma osmolality; (B) plasma AVP secretion correlated closely to plasma osmolality with a low osmotic threshold for AVP release; (C) nonsuppressible AVP secretion with normal osmotic release of AVP; (D) no abnormalities in AVP secretion. In this study, we found an entirely different type of AVP secretion from the above types in six patients with hyponatremia resulting from various causes during infusion of 5% hypertonic saline. To clarify the mechanism underlying the AVP secretion, we analyzed the interaction between osmotic and nonosmotic stimuli of AVP secretion in these patients. Despite hyponatremia, plasma AVP levels in all patients were not suppressed, which was attributed at least in part to the presence of nonosmotic stimuli for AVP release. These stimuli include nausea, hypotension, blood volume contraction, glucocorticoid deficiency or their combinations. Hypertonic saline infusion increased both serum sodium concentrations and plasma osmolality, although to subnormal levels, and concomitantly, alleviated some of the nonosmotic stimuli for AVP release formerly present in these patients. However, plasma AVP concentrations decreased rapidly during the infusion and reached the nadir in all patients. This phenomenon may be due to alleviation of nonosmotic stimuli for AVP release. Thus, the findings indicate that the potentiating effect of nonosmotic stimuli for AVP secretion may modify the osmotic regulation of AVP secretion in hypoosmolar state, resulting in the type of AVP secretion in this study.
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PMID:Interaction of osmotic and nonosmotic stimuli in regulation of vasopressin secretion in hypoosmolar state of man. 922 68

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

The aim of this study was to investigate the effect of vasopressin and long pulse-low frequency gastric electrical stimulation (GES) on gastric emptying, gastric and intestinal myoelectrical activity and symptoms in dogs. The study was performed in eight healthy female dogs implanted with four pairs of gastric serosal electrodes and two pairs of small bowel serosal electrodes, and a duodenal fistula for the assessment of gastric emptying. Each dog was studied in three sessions on three separate days in a randomized order with recordings of gastric and small bowel slow waves. Each study session consisted of 30-min baseline, 30-min stimulation and 30-min recovery period. In sessions 1 and 2, infusion of either saline or vasopressin (0.75 U kg(-1) in 30 mL saline instilled in 30 min) was given during the second 30-min period. The protocol of session 3 was the same as session 2 except long pulse-low frequency GES was performed during the second 30-min period. It was found that: (i) Vasopressin significantly delayed gastric emptying 30 and 45 min after meal and GES did not improve the vasopressin induced delayed gastric emptying; (ii) Vasopressin induced gastric dysrhythmias and GES significantly improved vasopressin induced gastric dysrhythmia; (iii) Vasopressin also induced intestinal slow wave abnormalities but GES had no effect on vasopressin induced small bowel dysrhythmia; (iv) Vasopressin induced symptoms and behaviours suggestive of nausea that were not improved by GES. We conclude that: (i) Vasopressin delays gastric emptying and induces gastric and small bowel dysrhythmias and symptoms in the fed state, and (ii) long pulse-low frequency GES normalizes vasopressin induced gastric dysrhythmia with no improvement in gastric emptying or symptoms.
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PMID:Effects of vasopressin and long pulse-low frequency gastric electrical stimulation on gastric emptying, gastric and intestinal myoelectrical activity and symptoms in dogs. 1578 43

Persistent hiccup can be a distressing disorder. I present a case of migraine-attack-associated sustained hiccup. Metoclopramide can swiftly control both hiccup and migraine headache. Vasopressin release probably underlies migraine-aborting action of metoclopramide while restoration of oesophageal smooth muscle function involves competitive dopaminergic antagonism and a prominent cholinergic agonist activity. Episodic prolonged hiccup associated with nausea is an unusual presenting feature of migraine.
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PMID:Metoclopramide for migraine-associated hiccup. 1670 Aug 63

Evidence of the effect of dehydration on physiological responses to hypoxia is limited. The purpose of this study was to determine the effect of hypohydration severity on physiological, renal hormonal and psychological responses to acute hypoxia. Eight males completed intermittent walking tests under normobaric hypoxic conditions (FI O(2) = 0.13) after completing four separate hypohydration protocols, causing change in body mass of approximately 0% (EU), -1% (H1), -2% (H2) and -3% (H3). Physiological and psychological markers were monitored throughout the 125 min test. Fluid controlling hormones were measured pre and post exposure. Heart rate, core temperature, peripheral arterial oxygen saturation (SpO(2)), minute ventilation and urine osmolality were found to be significantly different between hydration conditions and correlated with Lake Louise Questionnaire score (LLQ) (P < 0.05). LLQ score increased with hypohydration severity above H2 (EU 1.3 +/- 1; H1 1.2 +/- 1; H2 2.7 +/- 2; H3 3.9 +/- 2) (P < 0.001). Antidiuretic hormone and aldosterone increased over the test, but were not different between hydration conditions (P < 0.05). Atrial natriuretic peptide showed no change over time, or with conditions. Therefore, renal hormones are not influenced by hypohydration severity during moderate intensity hypoxic exercise. Hypohydration less than -2% induces greater physiological strain during hypoxic exercise and may cause rise in symptoms such as, fatigue, headache, nausea and lightheadedness.
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PMID:The effect of hypohydration severity on the physiological, psychological and renal hormonal responses to hypoxic exercise. 1919 72


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