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)

Antisera, with cross reactive antibodies removed by affinity chromatography, were used in the immunoperoxidase-bridge technique to study the distribution of oxytocin and vasopressin together with neurophysin in the hypothalamo-neurohypophysial system of the rat. The hormones were demonstrated in different areas of the supraoptic nucleus (SON) and paraventricular nucleus (PVN), in neurosecretory fibres of the hypothalamo-neurohypophysial tract, median eminence, and in nerve terminals of the neurohypophysis. Intact normal and rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain), and rats dehydrated by the administration of oral hypertonic saline were studied. In dehydrated rats the hormone concentration in the neurons, and the number of neurons containing hormone varied according to the time of dehydration stress. The observations support the hypotheses that: 1) oxytocin and oxytocin-neurophysin, and vasopressin and vasopressin-neurophysin are synthesised in different neurons and are transported along different axons; 2) the SON and PVN are functionally indistinguishable in that neurons containing oxytocin or vasopressin are present in both nuclei; and 3) the two types of neurons respond to osmotic stimulation in a way that is qualitatively the same but quantitatively different.
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PMID:Immunocytochemical study of the hypothalamo-neurohypophysial system. II. Distribution of neurophysin, vasopressin and oxytocin in the normal and osmotically stimulated rat. 32 53

A 32-year-old man developed panhypopituitarism and diabetes insipidus shortly after sustaining a head injury. Hormonal investigation showed that basal prolactin levels were moderately elevated the first two years after the accident, but later returned to normal. There was no rise in prolactin after administration on chlorpromazine, and the response to thyrotropin-releasing hormone was attenuated. Basal luteinizing hormone and follicle-stimulating hormone levels were low and there was no change after administration of luteinizing-hormone-releasing hormone. There was also no growth hormone elevation following arginine infusion. On the other hand, there was a normal but delayed elevation of thyrotropin in response to thyrotropin-releasing hormone. Appropriate stimulation tests showed normal responsiveness of the thyroid, adrenals and testes. These findings are compatible with an injury to the pituitary stalk, damaging the neurohypophyseal tract and affecting the blood supply to the pituitary gland.
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PMID:Pituitary insufficiency following head injury. 35 6

Angiotensin II is dipsogenic, and vasopressin (ADH) regulates renal water excretion. Together, these hormones govern overall mammalian water balance. The Brattleboro rat with inherited diabetes insipidus (DI) lacks ADH and is therefore a convenient model with which to elucidate mechanisms regulating water metabolism. In the present studies, angiotensin II has also been removed from DI rats by the administration of an inhibitor (captopril, SQ 14225; D-2-methyl-3-mercaptopropanoyl-L-proline) of the enzyme which converts angiotensin I, the relatively inert component of the renin-angiotensin system, to angiotensin II, the biologically active substance. SQ 14225 reduced the drinking rates, and after 6 days lowered peripheral plasma aldosterone concentrations were associated with hyperkalaemia. We conclude that the polydipsia of diabetes insipidus partly results from elevated plasma renin activities and angiotensin II concentrations seen in this syndrome. Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting.
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PMID:Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin. 38 37

The first known case of obstetric shock followed by diabetes insipidus without anterior pituitary deficiency is presented. A patient developed extreme thirst and polyuria after massive bleeding and prolonged shock due to placenta previa percreta with bladder invasion. Evaluation confirmed diabetes insipidus sensitive to vasopressin administration. Anterior pituitary deficiency could not be identified, either acutely or 6 months later.
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PMID:Diabetes insipidus following obstetric shock. 42 17

Pre- and postoperative evaluation of hypothalamic-pituitary function was performed in six children, aged 5.5 to 13.3 years with craniopharyngiomas. Before surgery growth hormone deficiency (GHD) was documented in four, hypothalamic hypothyroidism in three, and secondary ACTH-deficiency and hyperprolactinaemia in one patient. Diabetes insipidus was absent in all patients. After neurosurgical treatment GHD was present in all, hypothyroidism in five, ACTH-deficiency in three, hyperprolactinaemia in three, and diabetes insipidus in four children. The study shows that all endocrine functions tested may be defective even before surgery, although diabetes insipidus seems to be a rare preoperative complaint. Surgical intervention, however, often leads to additional endocrine disorders. From the data presented here one may suggest that TRH stimulation tests, evaluation of serum prolactin, and lysin-vasopressin stimulation tests are the most useful investigations to distinguish between hypothalamic and primary pituitary disorders.
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PMID:Pre- and postoperative evaluation of hypothalamo- pituitary function in children with craniopharyngiomas. 42 59

A case of assult with bilateral manual avulsion of the eyes was followed by highly selective infarction of the anterior hypothalamus. The hypothalamic infarction occurred as a result of avulsion of part of the optic chiasm together with the anterior perforating arteries passing through it; Following this assault, symptoms of hypothalamic dysfunction included altered thermoregulation, alternating diabetes insipidus, and inappropriate antidiuretic hormone (ADH) secretion, altered patterns of sleep and arousal, and changing cardiac arrhythmias. The case casts light upon the vascular supply of the human hypothalamus and on the degree of localization existing for various hypothalamic functions.
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PMID:Selective traumatic infarction of the human anterior hypothalamus. Clinical anatomical correlation. 43 Jan 59

The presence of vasopressin (VP) in pars distalis of rats and pigs was investigated. Using radioimmunoassay and bioassay of VP, a substance with immunological and biological properties of this hormone was found. This substance was not detected in the adenohypophysis of rats with diabetes insipidus. A partial purification of the VP-like peptide showed that it had the chromatographic and electrophoretic properties of VP. It could be identified with arginine vasopressin (AVP) in the case of the rat and lysine-vasopressin (LVP) in the case of the pig. In the Wistar strain, adrenalectomy induced progressively increasing concentrations of adenohypophysial VP. This increase was significant 15 days after surgery. It could be prevented by treatment with dexamethasone. These results indicate that the presence of VP in the anterior pituitary is related to the regulation of ACTH secretion.
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PMID:Evidence of vasopressin in adenohypophysis: research into its role in corticotrope activity. 43 70

We describe a patient with hypothalamic diabetes insipidus who after 20 years became refractory to the effect of commercial vasopressin injection. Vasopressin antibodies were measured using a sensitive hemagglutination technique. Resistance was associated with a high titer of antibodies that disappeared once vasopressin therapy was withdrawn and the diabetes insipidus was controlled with chlorpropamide. Antibodies were also measured in four additional patients with diabetes insipidus while they were or were not receiving vasopressin. A patient who had received the drug for only two years already had a substantial titer of antibodies to vasopressin, but in this case the response to the hormone was not impaired.
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PMID:Clinical resistance to vasopressin. Detection of antibody by hemagglutination. 44 72

In a prospective study of abnormalities of plasma sodium concentration carried out over one year 20 patients were identified who had a concentration exceeding 154 mmol(mEq)/1. Of these, eight patients had diabetes mellitus, eight had primary intracranial disorder, and four had become dehydrated. Five of the eight diabetics presented with hyperosmolar, non-ketotic precoma, and in all eight hypernatraemia developed despite treatment with hypotonic (0.45%) saline. There was a good correlation (r = -0.93) between the rates of change of plasma sodium and blood glucose concentrations, and thus a rise in plasma sodium concentration appeared to be a consequence of the treatment. In the early phase of treatment urinary sodium loss was extremely low despite a brisk diuresis, the infused sodium then predisposing the patients to hypernatraemia. All of the eight patients with intracranial disorders showed evidence of abnormal production of the antidiuretic hormone, six having frank diabetes insipidus. Severe hypernatraemia in this group was associated with a high mortality, fluid balance being difficult to maintain. Two of the four patients who had become dehydrated had had a recent gastrointestinal haemorrhage. In these patients infusion of 0.9% saline contributed to the hypernatraemia since urinary sodium loss was low. Severe hypernatraemia in adults is uncommon, but in established cases plasma and urinary biochemical indices should be measured frequently. Monitoring of the central venous pressure is usually necessary, and patients are best managed in an intensive care unit.
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PMID:Severe hypernatraemia in adults. 44 98

Despite the apparent absence of vasopressin (ADH), Brattleboro homozygotes [diabetes insipidus (DI) rats] can concentrate their urine when deprived of drinking water. Since other investigators have shown that reducing glomerular filtration rate (GFR) improves the concentrating ability of water-loaded dogs, the present studies were undertaken to quantify the magnitude and time course of changes in GFR during dehydration. Clearance experiments were performed in 10 conscious DI rats before and following 3, 6, 9, 12, 15, and 24 h of dehydration. Urine osmolality increased from 155.0 +/- 12.6 (SE) to 696.7 +/- 8.4 mosmol/kg H2O after 24 h. GFR averaged 984.3 +/- 79.6 microliters . min-1 . 100 g body wt-1 in the control phase, fell to about 80% of this value over the first 12 h of dehydration, and then declined to 27% at 24 h. The rats lost 20% of their body weight over the 24 h. The osmolality of the papillary tip averaged 896 +/- 44 mosmol/kg H2O at 24 h compared to a control value of 493 +/- 28. The lack of osmotic equilibration between urine and papillary interstitium suggests that dehydration did not appreciably increase the water permeability of the distal nephron. These experiments clearly show a progressive decline in GFR as urine becomes concentrated during dehydration in the absence of ADH; these events may or may not be causally related.
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PMID:Urinary concentrating ability during dehydration in the absence of vasopressin. 46 96


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