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)

Hyponatremia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) have been associated with several psychotropic drugs e.g., carbamazepine, neuroleptics, tricyclic antidepressants and more recently selective serotonin reuptake inhibiting (SSRI) antidepressants. SSRIs have gained widespread use in elderly depressed patients because of their favourable adverse effect profile. However, SSRIs have recently been associated increasingly with SIADH. We describe a 82-year old patient who was hospitalised after witnessed convulsions ten days after initiation of fluoxetine therapy for depression. She had hyponatremia and increased urine osmolarity suggesting SIADH. Using this case we discuss the clinical symptoms, aetiology, differential diagnosis and therapy of drug-induced SIADH.
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PMID:[SIADH with epileptic seizures and coma in fluoxetine therapy]. 1073 55

We report the case of a 62-year-old man who was administered sodium valproate (VPA) and who subsequently developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). He had been taking VPA for treatment of idiopathic generalized tonic-clonic convulsions since he was 56 years old. After substituting VPA with zonisamide, the serum sodium level returned to normal. We consider this episode of SIADH to be the result of a combination of factors including a weakness of the central nervous system and the long-term administration of VPA.
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PMID:Contribution of sodium valproate to the syndrome of inappropriate secretion of antidiuretic hormone. 1119 62

Pathogenesis of febrile convulsions (FC) is still unknown, suggested causes include the role of antidiuretic hormone (ADH). ADH is an endogenous antypyretic and his excessive production of the consequent hyponatraemia may be the cause of FC in children with susceptibility to this type of seizure. Whereas, interleukin-1 (IL1) is a pyrogenic substances and is involved in the release of AVP. Helminen et al. have reported a significantly higher production of IL1 in culture of peripheral blood monocytes stimulated with lipopolysaccharide (LPS) of children with FC than in the others with fever but without convulsions. More recently Lahat et al. have compared plasma and cerebrospinal fluid ILI levels of children with FC with those of children with fever but without convulsions, but they did not find significant differences. The aims of this study were to determine the IL1 levels in vivo and in the supernatants of cultures of peripheral blood mononuclear cells (PBMC) stimulated or not with LPS in children with FC and in children with fever without FC and to evaluate the influence of ADH and diazepam (DZ) on IL1 production. Blood samples for PBMC cultures were obtained from 11 children with FC on the hospital admission, (group 1) and after 48 hours from treatment with DZ (group 2). The production of IL1 was measured by RIA in the supernatants of the PBMC stimulated with LPS, LPS + DDAVP (synthetic vasopressin), LPS + DZ and in vivo in plasma samples. The control groups were constituted by 9 children with fever and without convulsions (group 3), 4 of them were studied at the end of fever too (group 4), and finally by 9 children in good health (group 5). No significant differences were observed. These results do not support the hypothesis that increased production of IL1 is involved in the pathogenesis of FC in children.
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PMID:[In vivo and in vitro production of interleukin-1 after febrile convulsions]. 1159 68

Activity of the magnocellular neurons that synthesize vasopressin in the supraoptic and paraventricular nuclei of the hypothalamus is modulated by local release of the neuropeptide within the nuclei. V(1a) and V(1b) vasopressin receptor genes are expressed in these cells. The present study reports the localization of V(1a) and V(1b) receptors using multiple labeling immunocytochemistry. Both receptors are mainly located in vasopressinergic magnocellular neurons and colocalized with vasopressin in cytoplasmic vesicles dispersed throughout the cell. Possible functional modifications of the mRNA and protein levels of the V(1a) receptor, the major isoform, were also investigated by semiquantitative in situ hybridization and immunocytochemistry in rats submitted to reduced or increased water intake. V(1a) mRNA and receptor levels varied with water balance. V(1a) mRNA level dropped in rats submitted to high water intake. Conversely, dehydration up-regulated the V(1a) receptor content. These observations suggest that the pathways that regulate the expression of the genes encoding vasopressin and the V(1a) receptor are linked, which fits the present findings that the two partners are colocalized in cytoplasmic vesicles. Colocalization might explain how V(1) autoreceptors are controlled by cell activity and/or local concentration of vasopressin (released locally by the neurons themselves), allowing fine adjustment of magnocellular neuron activity.
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PMID:The vasopressin receptors colocalize with vasopressin in the magnocellular neurons of the rat supraoptic nucleus and are modulated by water balance. 1179 98

This report addresses the verification of the hypothesis that arginine-vasopressin affects the formation of hyperthermia-evoked convulsions in early ontogenesis in rats on days 3, 5, 7, and 9 of postnatal life. The modification of experimental febrile convulsions by PACAP (pituitary adenylate cyclase-activating peptide) was investigated; PACAP is a physiological regulator of the neurosecretion of arginine-vasopressin. Arginine-vasopressin (10 microg/rat) and PACAP (0.01 microg/rat) decreased the latency of generalized tonic-clonic convulsions and the time of truncal generalization of convulsive activity on days 3 and 5 of rat development. Animals given arginine-vasopressin (0.1-10 microg/rat) sowed significant increases in the duration of generalized convulsions to the level of status epilepticus on day 9 of life. Conversely, administration of higher doses of PACAP (0.1 microg/rat) increased the threshold of tonic-clonic convulsions on days 3 and 5 and decreased it on days 7 and 9 of postnatal development. The indirect involvement of PACAP in the mechanisms of experimental febrile convulsions is suggested to act via changes in arginine-vasopressin neurosecretion.
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PMID:Peptidergic mechanisms of hyperthermia-evoked convulsions in rats in early postnatal ontogenesis. 1240 2

We report a child with diabetes insipidus and hypodipsia associated with holoprosencephaly. A two-year-old girl with the history of several admittances to hospital during and after the newborn period with hypernatremic dehydration, acute renal failure and convulsions is presented. The patient had hypodipsia, hypernatremia, microcephaly, failure to thrive, and unilateral cleft lip and palate. Magnetic resonance imaging revealed lobar type holoprosencephaly. Increased plasma osmolality and decreased urinary osmolality were detected. Her urine ADH level was 10 ng/day. Plasma osmolality levels returned to normal after hydration and administration of a vasopressin analogue. These findings suggest that in children with hypernatremia-hypodipsia syndrome, the possibility of cerebral malformations should always be kept in mind.
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PMID:Hypodipsia-hypernatremia syndrome associated with holoprosencephaly in a child: a case report. 1240 44

We present the case of a 6-week-old male infant who had a convulsion due to pertussis pneumonia. He was admitted to our emergency department because of lethargy and hypothermia. He developed a generalized tonic-clonic convulsion, requiring various treatments, including artificial ventilation. A chest CT showed bilateral pneumonia and laboratory data revealed hyponatremia with other features of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Although SIADH has been recognized as a cause of hyponatremia in association with pneumonia, there is little in the literature regarding SIADH caused by pertussis. Hyponatremia caused by SIADH must be considered as a differential diagnosis of seizures in pertussis infection of infants.
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PMID:Pertussis pneumonia complicated by a hyponatremic seizure. 1297 26

With an optical tweezer installed in our optical microscope we grab a single Madin Darby Canine kidney cell and keep it suspended in the medium without touching the glass substrate or other cells. Since the optically trapped cell remains with a closely round shape, we can directly measure its volume by using videomicroscopy with digital image analysis. We submit this cell to a hyperosmotic shock (up-shock) and video record the process: the cell initially shrinks due to osmotic efflux of water and after a while, due to regulatory volume increase (RVI), an osmoregulation response, it inflates again (water influx) until it reaches a new volume (the regulatory volume VR). In addition to considering standard osmotic water transport, we model RVI using a simple phenomenological model. We obtain an expression for cell volume variation as a function of time that fits very well with our experimental data, where two characteristic times appear naturally: one related to water transport and the other related to RVI. From the fit we obtain water permeability, osmolyte influx rate for RVI, and regulatory volume. With the addition of the hormone vasopressin, water permeability increases while the regulatory volume decreases until inhibition of RVI. In summary, we present a technique to measure directly volume changes of a single isolated kidney cell under osmotic shock and a phenomenological analysis of water transport that takes into account osmoregulation.
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PMID:Measurements and modeling of water transport and osmoregulation in a single kidney cell using optical tweezers and videomicroscopy. 1468 72

Hyponatremia caused by an inappropriately high level of antidiuretic hormone secretion after spinal surgery is an uncommon and self-limiting phenomenon that resolves within 2 or 3 weeks. During the early postoperative period, the patient's urine output and serum level of sodium should be monitored closely to prevent possible serious complications of the syndrome of inappropriate secretion of antidiuretic hormone. Symptoms vary depending on the severity of the hyponatremia and can range from mild headache, muscle cramps, nausea, and vomiting to convulsions, coma, and death. Treatment options include fluid restriction, oral intake of salt, and hypertonic saline. It is important that spine surgeons recognize this phenomenon early and treat it appropriately and conservatively to prevent possible serious complications.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone and hyponatremia after spinal surgery. 1519 39

In this review we first consider what information is carried by the activity of oxytocin cells. For these, as for many neuroendocrine neurones, synchronized bursting activity leading to pulsatile secretion is particularly important, and we consider possible mechanisms by which bursting may arise, and the role of intrinsic cell properties. Vasopressin cells also show a type of bursting behaviour, but their activity is not synchronized. We show how the behaviour of vasopressin cells fits a very simple dynamical systems model. Even structurally simple dynamical systems models can be computationally complex, with a rich repertoire of behaviour, and we show how the vasopressin cell model can be adapted and expanded to model the LHRH pulse generator network, and how the pituitary responsiveness to hypothalamic releasing factors may also be modelled with a different class of dynamical systems model.
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PMID:The origins and significance of pulsatility in hormone secretion from the pituitary. 1530 67


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