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)

Exercise-induced hyponatremia is commonly believed to be associated only with extraordinary physical efforts, or particularly strenuous exercise. Hyponatremia complicating moderate exercise has not been described previously. The authors describe the characteristics of seven patients with life-threatening hyponatremia associated with mild to moderate exercise. All patients suffered from nausea, vomiting, agitation, and confusion, appearing during or after moderate physical activity. Grand mal convulsions occurred in five of the patients. In laboratory results, hyponatremia was as low as 115 mEq/L, with a relatively high sodium concentration in the urine. High serum creatine kinase activity levels were found in most of the patients. All patients were discharged in good condition, without neurologic sequela. The authors conclude that hyponatremia is a possible complication of moderate exercise, and not only of endurance sports, and that exercise-induced hyponatremia can produce severe neurologic manifestations. The mechanism of the hyponatremia is unclear, but may be due to a hemodynamically inappropriate stimulus for antidiuretic hormone secretion.
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PMID:Case series: hyponatremia associated with moderate exercise. 861 81

Immaturity in water and electrolyte balance in the brain has been considered to increase the susceptibility of young animals and children to febrile convulsions (FCs). Arginine-vasopressin (AVP) is involved in the regulation of several centrally mediated events such as modulation of fever and the ease with which water permeates into and out of the brain. To evaluate the possible role of AVP in the control of water balance and susceptibility to convulsions during fever we measured the AVP concentration in the cerebrospinal fluid (CSF) and plasma of febrile children with or without convulsions. The febrile population consisted of 47 children, of whom 29 experienced seizures during fever. Seven children with epileptic symptoms and 18 children without seizures were included as nonfebrile controls. The CSF AVP concentration in febrile children without seizures and in nonfebrile convulsive children was significantly lower (0.60 +/- 0.07 pmol/l, mean +/- SEM, P < 0.01 and 0.65 +/- 0.19 pmol/l, P < 0.05, respectively) than in nonfebrile children without convulsions (0.83 +/- 0.06 pmol/l). However, the levels of CSF AVP were not significantly different in children with FCs (0.71 +/- 0.06 pmol/l) compared with other groups. CSF AVP correlated with the CSF osmolality (r = 0.33, P = 0.02). No statistical differences in plasma AVP levels between the groups could be found. The present data provide support for the hypothesis of synchronous regulation of osmolality and AVP concentration in CSF. During fever the concentration of CSF AVP was lower in nonconvulsive children compared with nonfebrile nonconvulsive children. CSF AVP levels were not affected in febrile children by convulsions.
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PMID:Vasopressin in the cerebrospinal fluid of febrile children with or without seizures. 873

We have examined the fluorescence intensity decays of oxytocin and [Arg8]-vasopressin resulting from the single tyrosyl residue in each peptide, and the intensity decay of the Asu1,6-analogues in which the disulfide bridge is substituted by a CH2-CH2 bridge. Viscosity-dependent steady state and intensity decay measurements indicated that fluorescence resonance energy transfer (FRET) from tyrosyl phenol to the disulfide bridge is responsible for the decrease in fluorescence relative to the Asu-analogues. The frequency-domain phase and modulation data for the tyrosyl donor were interpreted in terms of fluorescence resonance energy transfer (FRET) to the weakly absorbing disulfide bridge and a distribution of donor-to-acceptor distances. Energy transfer efficiencies were determined from both time-resolved and steady-state measurements. Fitting the frequency-domain phase and modulation data to a Gaussian distance distribution indicated that the average inter-chromophoric distance (Rav) is similar in both compounds, Rav = 7.94 A for oxytocin and Rav = 8.00 A for vasopressin. However, the width of the distance distribution is narrower for vasopression (hw = 2.80 A) than for oxytocin (hw = 3.58 A), which is consistent with restriction of the tyrosine phenol motion due to its stacking wih the Phe3 side chain of vasopressin. Finally, the recovered distance distribution functions are compared with histograms describing the distance between the chromophores during the course of long, in vacuo, molecular dynamics runs using the computer program CHARMm and the QUANTA 3.0 parameters.
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PMID:Distance distributions from the tyrosyl to disulfide residues in the oxytocin and [Arg8]-vasopressin measured using frequency-domain fluorescence resonance energy transfer. 885 63

A prospective observational study of the pathophysiology of sodium and water disorders in patients with pituitary region tumours after surgical excision was carried out in 20 patients. Serial pre-operative and post-operative fluid and sodium balance, plasma and urine elctrolyte biochemistry and their derived parameters, and circulating hormones associated with fluid balance, atrial natriureic peptide (ANP) and antidiuretic hormone (ADH) were documented to correlate with the patients' clinical conditions. Ten out of these twenty cases developed diabetes insipidus (DI) requiring ADH replacement therapy, although in the majority (6 cases), this way only a transient event. Of the nine patients who developed hyponatraemia, six had symptoms such as impaired consciousness and convulsions. Four patients developed alternating hypoatraemia and hypernatraemia, which constituted a difficult group, where appropriate sodium and fluid management, and ADH replacement therapy were based upon twice daily plasma and urine biochemistry and their derived parameters. Whilst DI in this group of patients was the result of a low circulating ADH level, hyponatraemia was not associated with an exaggerated ADH activity (6.0 +/- 2.3 vs 7.4 +/- 2.3 pmol/ml, mean +/- SEM). Rather, hyponatraemia was strongly associated with an elevated circulating ANP concentration (82.4 +/- 10.5 vs 30.0 +/- 3.1 pmol/ml, mean +/- SEM, p < 0.001), resulting in salt wasting and hypovolaemia.
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PMID:Water and sodium disorders following surgical excision of pituitary region tumours. 889 Sep 88

One-hundred-and-thirty-six children below 12 years of age hospitalized with a diagnosis of tuberculous meningitis (TBM) have been investigated to identify the underlying cause of convulsions. One-hundred-and-one children (74 per cent) presented with seizures before and/or during hospitalization. Generalized tonic and clonic seizures (GTCS) were the commonest (58 per cent) type of seizures followed by focal seizures (FS) (38 per cent) and tonic spasms (TS) (4 per cent). EEG changes were more frequently observed in cases with FS and in those children with GTCS who presented after first week of hospitalization. EEG findings included generalized dysrythmia with paroxysmal slow activity (38 per cent), interhemispheric asymmetry (23 per cent), multiple spike and wave pattern (10 per cent), and focal spike and wave pattern (15 per cent). CT scan findings were more common in those children with GTCS and TS who presented with recurrent seizures and/or seizures manifesting after first week of hospitalization. FS presenting at any stage of the disease were associated with CT scan abnormalities. Abnormalities detected in CT scan of brain included meningeal enhancement (55 per cent), hydrocephalus (32 per cent), tuberculomas (27 per cent), and cerebral infarctions (13 per cent). Clinical presentation and investigations indicate that the probable cause of convulsions could be attributed to cerebral edema (57 per cent), syndrome of inappropriate secretion of antidiuretic hormone (35 per cent), hydrocephalus (32 per cent), tuberculoma (27 per cent), abnormal electric focus (25 per cent), and cerebral infarction (13 per cent).
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PMID:Convulsions in tuberculous meningitis. 898 21

Water intoxication is a serious condition which may be caused by desmopressin overdose, with reversible or irreversible neurological complications. In the past, desmopressin was used in endocrinological centers for the treatment of antidiuretic hormone deficiency (central diabetes insipidus). Indications for hormone treatment have since widened, especially as an effective solution for nocturnal enuresis. It is now often prescribed in community clinics, and its use has been encouraged by extensive promotion. We describe a 15-year-old boy with primary nocturnal enuresis who started treatment with desmopressin 1 year prior to admission. He was allowed to use the drug without supervision, and drank excessively. The result was water intoxication which required admission for intensive care because of loss of consciousness and convulsions for 36 hours.
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PMID:[Water intoxication following desmopressin overdose]. 915 15

Fourteen infants with severe acute bronchiolitis were admitted to the Intensive Care Unit (ICU) of Tunis. This pathology represents 36% of severe bronchopulmonary infections admitted to this ICU. Their age ranged between 2 and 48 weeks (mean: 15 weeks). Eight infants had hypotrophy. Two infants had congenital heart disease and one infant had tracheo-bronchomalacia. Viruses were found in 6/11 patients. Respiratory syncytial virus (RSV) was identified in five patients and an adenovirus in one patient. Five patients had respiratory arrest at ICU admission. Ten infants had evidence of atelectasis on chest X-ray films. Thirteen patients required mechanical ventilation. One infant had inappropriate antidiuretic hormone secretion resulting in convulsions. One infant had supraventricular tachycardia. Both had RSV infection. One patient who had congenital heart disease and RSV infection died. In the other 12 patients receiving mechanical ventilation, the mean duration of ventilation was 9 days (range: 2-30 days). The second patient who had congenital heart disease and RSV infection had severe respiratory sequelae at discharge.
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PMID:[Clinical, therapeutic and developmental aspects of acute bronchiolitis in Tunisia]. 918 23

Recent work has demonstrated that the brain has the capacity to synthesize impressive amounts of the gases nitric oxide (NO) and carbon monoxide (CO). There is growing evidence that these gaseous molecules function as novel neural messengers in the brain. This article reviews the pertinent literature concerning the putative role of NO and CO as critical neurotransmitters and biological mediators of the neuroendocrine axis. Abundant evidence is presented which suggests that NO has an important role in the control of reproduction due to its ability to control GnRH secretion from the hypothalamus. NO potently stimulates GnRH secretion and also appears to mediate the action of one of the major transmitters controlling GnRH secretion, glutamate. Evidence is presented which suggests that NO stimulates GnRH release due to its ability to modulate the heme-containing enzyme, guanylate cyclase, which leads to enhanced production of the second messenger molecule, cGMP. A physiological role for NO in the preovulatory LH surge was also evidenced by findings that inhibitors and antisense oligonucleotides to nitric oxide synthase (NOS) attenuate the steroid-induced and preovulatory LH surge. CO may also play a role in stimulating GnRH secretion as heme molecules stimulate GnRH release in vitro, an effect which requires heme oxygenase activity and is blocked by the gaseous scavenger molecule, hemoglobin. Evidence is also reviewed which suggests that NO acts to restrain the hypothalamic-pituitary-adrenal (HPA) axis, as it inhibits HPA stimulation by various stimulants such as interleukin-1 beta, vasopressin, and inflammation. This effect fits a proinflammatory role of NO as it leads to suppression of the release of the anti-inflammatory corticosteroids from the adrenal. Although not as intensely studied as NO, CO has been shown to suppress stimulated CRH release and may also function to restrain the HPA axis. Evidence implicating NO in the control of prolactin and growth hormone secretion is also reviewed and discussed, as is the possible role of NO acting directly at the anterior pituitary. Taken as a whole, the current data suggest that the diffusible gases, NO and CO, act as novel transmitters in the neuroendocrine axis and mediate a variety of important neuroendocrine functions.
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PMID:Gaseous transmitters and neuroendocrine regulation. 920

Subcutaneously (s.c.) administered [Arg8]vasopressin (AVP) potentiated seizures induced by intracerebroventricular (i.c.v.) injection of 1.95 mg pilocarpine (a muscarinic cholinergic agonist). A bell-shaped relation between dose and effect was found. I.c.v. pretreatment with a V1, V2 or oxytocin receptor antagonist was performed to determine whether and what type of receptor is involved in this proconvulsive effect of vasopressin. For these experiments a higher dose of pilocarpine (2.4 mg i.c.v.) was injected. This caused seizures in a slightly but not significantly higher percentage of the rats. A dose-dependent protective action of the V2 receptor antagonist d(CH2),[D-Ile2,Ile4]AVP (effective doses were 25 and 125 ng) on seizures was found. A reduction was observed in the number of animals that developed tonic-clonic convulsions. Neither the V1 receptor antagonist d(CH2)5[Tyr(Me)2]AVP nor the oxytocin receptor antagonist desGly(NH2)9d(CH2)5[Tyr(Me)2Thr4]OVT possessed anti-convulsive activity. Subsequently the type of receptor was studied in detail with fragments of AVP with either V1 or V2 activity. AVP (with V1 and V2 affinity) (1 and 3 microg s.c.) potentiated pilocarpine (1.95 mg) induced seizures. Vasotocin and oxytocin were without effect. Interestingly neither s.c. nor i.c.v. administration of the selective kidney type vasopressin receptor (V2) agonist dDAVP potentiated pilocarpine induced seizures. Several selective antidiuretic agonists (V2), such as d[Val4]AVP, d[Phe2,Val4,D-Arg8]vasopressin (3 microg), [Val4,D-Arg8]vasopressin (3 microg) and d[Val4,D-Arg8]vasopressin (3 microg) were active. Other selective antidiuretic compounds, such as [Val4]AVP, dAVP, d[Tyr(Me)2]AVP and HO[D-Arg8]vasopressin (3 microg) did not influence seizures. These results demonstrate that a combination of substitution of aminoacid 4 (Gln) by Val and to a lesser extent deamination and the D-arginine form yield an active molecule, which can potentiate pilocarpine induced seizures and suggest the existence of a V2 receptor subtype in the brain.
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PMID:Proconvulsive effect of vasopressin; mediation by a putative V2 receptor subtype in the central nervous system. 921 58

An 11-year-old girl presented with a syndrome of inappropriate antidiuretic hormone secretion, which was transitory and, initially, of obscure origin. Subsequently, the patient's hypothalamic disorder emerged as a component of a steroid-responsive relapsing encephalomyelitis with cerebral pathology restricted to the basal ganglia and brainstem. Where such a disorder fits in the spectrum from acute disseminating encephalomeylitis to multiple sclerosis is discussed.
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PMID:An 11-year-old girl with syndrome of inappropriate antidiuretic hormone secretion. 1052 40


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