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)

When vasopressin is administered into the lateral ventricles of rats it produces severe convulsive activity characterized by a rapid barrel rotation. Electrical recordings from the dorsal hippocampus indicate marked elevations in the amplitude and frequency at doses of 5 microliter of 2 x 10(-5) M vasopressin. No significant behavioral effects were noted with oxytocin, somatostatin, beta-melanophore-stimulating hormone, adrenocorticotropin, or leu-enkephalin. Pretreatment of the rats with intraventricularly administered oxytocin, beta-MSH, or systemically administered Dilantin prevented the vasopressin-induced seizures. With the use of chemical and enzymic modification procedures, the essential fragment and amino acids of vasopressin needed for the activity were determined. It was concluded that although the peptide could be acting by vasoconstricting blood arterioles and capillaries in the brain, it may also be exerting a direct excitatory action on neurons.
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PMID:Chemical requirements of vasopressins for barrel rotation convulsions and reversal by oxytocin. 740 Nov 98

The authors report the frequency, characteristic clinical symptoms, laboratory alterations and diagnostic criteria of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after subarachnoid haemorrhage. The data on 290 patients with subarachnoid haemorrhage (SAH) during a period of years at the Division of Neurosurgery, University Medical School, Szeged, are analysed. Twenty-seven (9.3%) patients developed SIADH. Thirteen (4.5%) patients had severe and 14 (4.8%) had mild SIADH. The problems of the treatment are discussed in detail and the different therapeutic methods are listed: NaCl infusion, water withdrawal and administration of Dilantin, diuretics, mineralocorticosteroids, lithium and demeclocycline. The undesirable side-effects observed accompanying various therapeutic regimen are analysed. The introduction of V2 antagonists into clinical practice appears to be a most perspective procedure. For study of the pathogenesis of SIADH following SAH, the possibility of treatment with V2 antagonists on an experimental model of SAH in rat was created. A significant water retention and increases in brain water and sodium content were observed in rats with SAH. Plasma AVP levels were also elevated after SAH. AVP plays an important role in the development of antidiuresis following water loading and disturbance of the brain water and electrolyte balance after SAH. Water retention and the higher brain water and sodium accumulation could be totally prevented by administration of a V2 antagonist. These results demonstrate that cerebral oedema generated by artificial cerebral bleeding in rats is significantly reduced following the administration of a highly specific V2 antagonist, suggesting a new approach to the treatment of SIADH.
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PMID:Cerebral oedema after subarachnoid haemorrhage. Pathogenetic significance of vasopressin. 874 54