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

A 29-year-old nullipara was admitted at 31 weeks' gestation because of toxemia. She noted gradually polyuria, severe thirst, malaise, nausea and anorexia. A water-deprivation test and administration of aqueous vasopressin confirmed the diagnosis of nephrogenic diabetes insipidus. At 33 weeks' gestation, blood chemistry studies revealed moderately elevated transaminase levels and hyperuricemia. Male twins were delivered by vacuum extraction at 35 weeks' gestation. After delivery, she became drousy and icterus appeared. Acute hepatic failure with marked hyperuricemia was diagnosed. She was treated with glucose solution with glucagon and soluble insulin, branched chain amino acids, gabexate mesilate, lactulose and famotidine. Her consciousness cleared rapidly and all laboratory data became normal by 15 days postpartum. The urine volume was about 5 liters per day from the first to sixth postpartum day. The diuresis decreased after the eighth postpartum day. Rare pregnancy complicated by transient nephrogenic diabetes insipidus and acute hepatic failure is discussed.
 ...
PMID:Transient nephrogenic diabetes insipidus associated with acute hepatic failure in pregnancy. 365 42

Administration of cholecystokinin (CCK) to rats caused a dose-dependent increase in plasma levels of the neurohypophyseal hormone oxytocin (OT). The OT secretion was comparable to that found in response to nausea-producing chemical agents that cause learned taste aversions. The effect of CCK on OT secretion was blunted after gastric vagotomy, as was the inhibition of food intake induced by CCK. Food ingestion also led to elevated plasma OT in rats, but CCK and aversive agents caused even greater OT stimulation. Thus, after administration of large doses of CCK, vagally mediated activation of central nausea pathways seems to be predominantly responsible for the subsequent decrease in food intake. Despite their dissimilar affective states, both nausea and satiety may activate a common hypothalamic oxytocinergic pathway that controls the inhibition of ingestion.
 ...
PMID:Oxytocin secretion in response to cholecystokinin and food: differentiation of nausea from satiety. 371 53

Seven male volunteers were given apomorphine (14-20 micrograms/kg) subcutaneously on a total of ten occasions. Nausea was experienced on six occasions and on four occasions there was no effect. Venous samples were taken before injection, at peak nausea and 20 min later for assay of factor VIII coagulant activity (FVIIIC), von Willebrand factor antigen (vWFAg), the ristocetin cofactor (FVIIIRiCof), euglobulin clot lysis time (ECLT), fibrinopeptide A (FPA), FPA generation time, activated partial thromboplastin time (APTT), vasopressin (aVP) and adrenaline. During nausea plasma aVP concentrations rose from median values of 0.4 pg/ml (at time 0) to 76 pg/ml at peak nausea and fell to 32 pg/ml 20 min later. Adrenaline rose from 0.36 to 0.91 nmol/l (P less than 0.05) before falling to 0.55 nmol/l. During nausea, FVIIIC rose from 100% to 143% (P less than 0.05) and to 214% (P less than 0.05) 20 min later. FVIIIRiCof and vWFAg showed similar changes. Plasminogen activator activity (10(6)/ECLT2) rose from 23 units at time 0 to 592 units during nausea and 1135 units (P less than 0.05) after 20 min. The APTT fell from 49 s to 44 s during the study, plasma FPA levels and the FPA generation time both remained unchanged. On the four occasions nausea was not experienced, there were no changes in vasopressin and catecholamine concentrations nor in haemostatic function. During the study, plasma aVP concentrations rose to levels previously shown to influence haemostatic function. This provides further support for the view that aVP has a secondary role as a mediator of acute changes in haemostasis, and during nausea contributes with adrenaline to an abrupt change in factor VIII and fibrinolytic activator activity.
 ...
PMID:Vasopressin and catecholamine secretion during apomorphine-induced nausea mediate acute changes in haemostatic function in man. 376 10

The responses of plasma and ventricular cerebrospinal fluid (CSF) vasopressin concentration to dehydration, postural changes, and induction of nausea were studied in 21 patients with hydrocephalus of various etiology. The 24-h dehydration test evoked a significant increase in plasma osmolality and vasopressin concentration, whereas the concentration of vasopressin in CSF was unchanged. Head-up tilt to 50 degrees for 45 min with a tilt bed resulted in a modest increase of plasma vasopressin in patients who did not develop presyncopal symptoms, but no changes were seen in CSF vasopressin. Induction of nausea by subcutaneously injected apomorphine provoked a marked (20- to 50-fold) rise in plasma vasopressin concentration within 15 min, and the plasma concentration was significantly increased above base-line values for 60-120 min. Despite the prolonged period of high plasma vasopressin concentration CSF vasopressin was not influenced by the apomorphine injection. The findings suggest that the concentration of vasopressin in the CSF is controlled by mechanisms other than the well-known osmotic and nonosmotic stimuli of vasopressin release into the blood.
 ...
PMID:Vasopressin in plasma and ventricular cerebrospinal fluid during dehydration, postural changes, and nausea. 397 Jan 88

Baseline plasma vasopressin concentrations were measured in 10 healthy women during a normal menstrual cycle, 97 normal women during pregnancy and 43 pregnant women hospitalized during the third trimester because of pregnancy-induced hypertension (PIH). Plasma vasopressin levels were also measured in 44 normal pregnant women in early labor and in 30 parturients at delivery. The random plasma vasopressin concentrations did not vary significantly between the nonpregnant women during the follicular phase (2.3 +/- 0.2 microU/ml) and luteal phase (2.2 +/- 0.3 microU/ml) or during the third trimester in normal pregnant women (2.0 +/- 0.2 microU/ml) or those with PIH (2.0 +/- 0.1 microU/ml). There was a significant reduction (p less than 0.01) in plasma vasopressin levels in the pregnant women during the first trimester (1.5 +/- 0.1 microU/ml) and second trimester (1.5 +/- 0.1 microU/ml) as compared to levels in nonpregnant and pregnant women in the third trimester. The mean plasma vasopressin levels in the pregnant women complaining of nausea were similar to those in the pregnant women without nausea. Plasma vasopressin levels in women during labor did not increase significantly over third-trimester-pregnancy concentrations during the first stage of labor (1.9 +/- 0.1 microU/ml) or at delivery (1.8 +/- 0.1 microU/ml). These cross-sectional measurements of maternal plasma vasopressin levels do not support a role for vasopressin in the development of PIH or in the initiation or maintenance of labor.
 ...
PMID:Vasopressin levels during pregnancy and labor. 400 48

The syndrome of tumor-induced osteomalacia has been previously thought to occur only in association with mesenchymal tumors, although one report has linked prostatic carcinoma with the syndrome. We report the case of a patient who presented first with the clinical and biochemical features of the syndrome of inappropriate antidiuretic hormone secretion, and then oncogenic osteomalacia. The first syndrome was characterized by headaches, nausea, and vomiting; serum sodium determinations ranged between 107 and 118 meq/L with simultaneous urine spot sodium concentrations of 100 to 116 meq/L. The circulating antidiuretic hormone level was markedly elevated to 261.5 microU/mL. The osteomalacia was discovered incidentally when depressed serum phosphorus levels of 1.2 to 1.7 mg/dL were noted in association with 24-hour urine phosphorus excretion exceeding 1000 mg/24 h. Undecalcified tetracycline-labeled bone biopsy samples confirmed oncogenic osteomalacia. Only afterward was a small-cell carcinoma of the lung identified as the likely source of both of these syndromes.
 ...
PMID:Oncogenic osteomalacia and inappropriate antidiuretic hormone secretion due to oat-cell carcinoma. 609 61

Digoxin acts at central neural (CNS) as well as peripheral sites after intravenous administration. In contrast, the analog, 3-beta-O(4-amino-4,6-dideoxy-beta-D-galactopyranosyl)-digitoxigenin (ASI-222), cannot cross the blood-brain barrier so it acts only at sites outside the CNS. The effects of these two agents on plasma antidiuretic hormone activity (ADH) were investigated in conscious dogs. Despite previous evidence that digoxin produces reflex decreases in sympathetic nerve activity by activating ventricular receptors with vagal afferents, no decreases in ADH were detected when either digoxin (25 and 50 micrograms/kg) or ASI-222 (38.5 micrograms/kg) were administered intravenously even with preexisting high levels of plasma ADH. In contrast, both digoxin (50 micrograms/kg) and ASI-222 (38.5 micrograms/kg) resulted in increased ADH levels, but only in association with emesis and behavioral changes suggestive of nausea. Cerebroventricular (IVT) injections of digoxin were given, starting with a dose of 0.1 microgram, that were intended to produce a comparable cerebrospinal fluid (CSF) concentration to that associated with the 50 micrograms/kg intravenous dose. Only the highest dose of digoxin, 1 micrograms, but not 0.1 and 0.3 micrograms, produced increases in ADH and emesis when given into the lateral cerebral ventricle. This is further evidence that a site accessible to blood but not to CSF was involved. These results suggest that digoxin and ASI-222 may activate pathways in the area postrema and produce increases in ADH as well as emesis.
 ...
PMID:Effect of digoxin and amino sugar cardiac glycoside (ASI-222) on plasma antidiuretic hormone activity. 618 2

6 patients with amyotrophic lateral sclerosis were treated with intravenous infusion of 100-200 million IU per day of human leukocyte interferon. Side effects of treatment included fever, chills, malaise, nausea, marked leukopenia, mild anemia, and thrombocytopenia. Tiredness, confusion, papilledema, and overall signs of acute encephalitis were observed. Tendon reflexes and muscle force decreased. EEG activity was slowed, and evoked potentials showed significant slowing of conduction times. Neuropsychological tests revealed congitive dysfunction. The syndrome of inappropriate antidiuretic hormone secretion developed in all patients. All side effects were reversible with cessation of interferon treatment.
 ...
PMID:Neurotoxic and other side effects of high-dose interferon in amyotrophic lateral sclerosis. 620 81

Twelve male volunteers given apomorphine (20 micrograms/kg/hr) for 40 min by i.v. infusion had significant changes in growth hormone, prolactin, vasopressin, pulse rate, sedation and nausea. Naloxone, (20 mg i.v.) or placebo given in a double-blind manner 10 min before the end of the apomorphine infusion as a concealed bolus did not alter the effects of apomorphine. Vasopressin rise correlated significantly with nausea intensity. We conclude that acute opiate receptor blockade does not reverse most apomorphine effects.
 ...
PMID:Failure of naloxone to reverse apomorphine effects in humans. 630 2

Hyponatremia and hypo-osmolality developed in a 70-year-old patient. It was probably mediated by hypersecretion of antidiuretic hormone, which, in turn, was due to prolonged nausea and vomiting. Severe esophagitis was the cause of the nausea. The patient was not given large amounts of fluids intravenously, and it is likely that she continued to drink for nondipsetic reasons. In view of her medical history of neurosyphilis, the possibility of a disturbance in the mechanism of thirst regulation is discussed, but remains unproved.
 ...
PMID:Hypo-osmolal syndrome due to prolonged nausea. 669 59


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>