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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intermittent hypernatremia following hypothalamic surgery or trauma is usually attributed to the triphasic dysfunction of vasopressin release (diabetes insipidus, inappropriate vasopressin release, and diabetes insipidus). A 39-year-old patient had hypodipsia and intermittent hypernatremia following hypothalamic surgery for a chromophobe adenoma. Mean arterial pressure fell by 25 percent during orthostasis testing and was associated with an increase in vasopressin levels from 1.3 microU/ml to 12 microU/ml. Plasma renin activity and aldosterone increased from 1.1 to 16 ng/ml per hour and from 6.7 to 39 ng/dl, respectively, and remained elevated for three and a half hours after tilt testing. Hypertonic saline infusion, on the other hand, increased serum osmolality from 290 to 304 mOsm/kg but did not result in a significant rise in vasopressin levels (all were less than 1 microU/ml). These results are consistent with a selective dysfunction of the osmoreceptor pathways of vasopressin release and intact volume receptor-mediated pathways. Patients with intermittent hypernatremia following hypothalamic surgery or trauma should be questioned specifically regarding thirst. If it is impaired or absent, these patients should be watched carefully, not only for the development of triphasic dysfunction of vasopressin release, but also for a selective osmoreceptor dysfunction associated with thirst deficits as found in patients with "essential hypernatremia."
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PMID:Selective osmoreceptor dysfunction presenting as intermittent hypernatremia following surgery for a pituitary chromophobe adenoma. 372 18

We describe a 30 year old man who developed chronic adipsic hypernatraemia and hypothermia following a subarachnoid haemorrhage from an anterior communicating artery aneurysm. Anterior pituitary function tests were normal. Hypothermia was demonstrated over 4 years with loss of the ability to control heat conservation despite body temperatures as low as 30 degrees C. He failed to experience thirst despite plasma sodium concentrations of up to 187 nmol/l and plasma osmolalities of up to 397 mOsm/kg. The slope of the plasma vasopressin-plasma osmolality curve indicated loss of the osmoreceptor. There was an absent vasopressin response to insulin-induced hypoglycaemia but a normal response to apomorphine. The apomorphine-stimulated immunoreactive vasopressin was shown to behave identically to the synthetic peptide on HPLC and was bioactive.
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PMID:Chronic hypernatraemia and hypothermia following subarachnoid haemorrhage. 377 77

Patients with essential hypernatremia maintain urinary concentrating ability despite plasma hyperosmolality and low plasma vasopressin concentrations. We investigated renal sensitivity to ultralow dose vasopressin infusions in two patients with a syndrome of hypodipsia, hypernatremia with selective osmoreceptor dysfunction, early puberty, and aggressive behavior. The patients were water loaded until a hypotonic diuresis was established. Vasopressin was infused in stepwise increments from 0.4-12 fmol/kg X min. Both patients had increased renal sensitivity to vasopressin, achieving negative free water clearance at infusion rates of 0.4 and 4 fmol/kg X min (normal greater than or equal to 6). Treatment for 3 months with 1-desamino-8-D-arginine vasopressin (DDAVP) led to an improvement in behavior and the reporting, for the first time, of a sensation of thirst. After DDAVP therapy both patients had a reduction of their renal sensitivity to infused vasopressin. We conclude that untreated patients with essential hypernatremia have increased renal sensitivity to vasopressin which is reduced by DDAVP administration.
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PMID:Increased renal sensitivity to vasopressin in two patients with essential hypernatremia. 378 33

A review is given on symptoms, etiology, pathogenesis and prognosis of central pontine myelinolysis (CPM). Since 1959, 315 cases of CPM have been reported in world literature, 41 per cent of the patients described developed their neurological symptoms in the course of chronic alcoholism. In about 32 per cent CPM was connected with electrolyte disturbance, especially hypo- or hypernatremia. Beside the complications of alcoholism, accompanying diseases were malignancies (9%) infections of the lung (10%) and diseases of the central nervous system (7%). Current theories about etiology and pathogenesis of CPM are reviewed with special reference to the syndrome of inappropriate secretion of the antidiuretic hormone (IADH). Own experiences with clinical diagnosis of CPM are reported. Seven patients with neurological symptoms in hyponatremia have been seen prospectively during one year. In three cases clinically, in one patient neuropathologically the diagnosis of CPM was made.
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PMID:[Central pontine myelinolysis]. 380 30

A patient exhibited brain damage, polyuria, and refractory hypernatremia after myocardial infarction and cardiopulmonary arrest. Serum vasopressin levels were relatively fixed and inappropriately low for the elevated serum osmolality. Hypernatremia persisted despite administration of vasopressin; after vasopressin was discontinued, serum sodium value was corrected with small doses of furosemide and replacement of free water. In her case, impairment of osmotic homeostasis could not be attributed to either simple resetting or complete destruction of osmoreceptors; metabolic normalization required an unusual therapeutic approach.
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PMID:Polyuria and refractory hypernatremia after cardiopulmonary arrest. 381 34

Hypernatraemic states are associated with an increased risk of thrombosis. To examine the relative contributions of sodium and vasopressin, we infused hypertonic saline in 11 male volunteers and measured the effect on factor VIII (FVIII), euglobulin clot lysis time (ELT) and fibrinopeptide A (FPA) generation. Samples were taken pre-infusion, hourly during a 3h infusion of 450 ml 6M saline and one hour after the infusion had stopped. Mean plasma osmolality (SEM) rose from 287(0.7) to 302(10) mOsm after 3h (p less than 0.01). Plasma vasopressin concentrations rose from 1.0(0.3) to 4(0.94) pg/ml over 3 hr (p 0.01). Plasminogen activator activity (10(6)/ELT2) rose from 65(10) to 372(55) units (p less than 0.001). There was a highly significant correlation between plasma osmolality and plasminogen activator activity (r = 0.5 p less than 0.0001). FPA generation time shortened from 7.2(0.4) to 5.4(0.6) min after 2h and 5.3(0.6) after 4h (n = 6). Values for FPA after 4 min incubation steadily increased from 5.8(1.2) to 14.3(4.6) pmol/ml during the infusion but differences failed to achieve statistical significance. FVIIIC (1 stage) remained constant at 75(5.5%) during the infusion. There was a small and statistically insignificant increase in FVIII RiCof after 3h and FVIII RAg decreased slightly. The results suggest that hypernatraemia and increasing plasma aVP concentrations produce changes in haemostatic function consistent with a hypercoaguable state. The mechanisms for the effect are unclear. These changes in haemostatic function might contribute to the thrombo-embolic complications of conditions such as hyperosmolar coma in diabetes mellitus or severe heatstroke in which degrees of hypernatraemia occur.
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PMID:Does hypernatraemia promote thrombosis? 393 26

Two unrelated boys (C.C. 13 years; J.W. 18 years) presenting with early puberty and episodes of aggressive behaviour were found to have hypernatraemia and hypodipsia. Plasma vasopressin (AVP) levels were inappropriately low in relation to plasma osmolality, but the patients did not have diabetes insipidus since 24 h urinary volumes were less than 1 litre and the maximal urinary osmolality was 1232 in C.C. and 950 in J.W. Plasma renin activity was elevated (greater than 2000 mg AI/1/h) although aldosterone concentrations were normal. Excretion of a water load (20 ml/kg) was delayed, but plasma renin and aldosterone fell with increased naturesis. An infusion of 0.85 mol/l saline produced a rise in AVP in C.C. but not in J.W. Insulin and hypotension resulted in the release of AVP in both boys suggesting a selective defect of osmoreceptor function. Hyperprolactinaemia and an exaggerated PRL response to TRH were also noted but no intracranial lesion was demonstrable on CT scan. These boys appear to have a hypothalamic syndrome with early puberty, hyperprolactinaemia, hypodipsia and osmoreceptor dysfunction which may be associated with aggressive behaviour.
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PMID:Lack of thirst, osmoreceptor dysfunction, early puberty and abnormally aggressive behaviour in two boys. 398 68

We describe a 24-year-old short, obese girl who has bizarre episodic neurological abnormalities related to hyperosmolality due to hypernatraemia. Investigation of osmoregulation by water loading and infusion of hypertonic saline revealed (i) hypodipsia with thirst onset raised to plasma osmolality of 332 mmol/kg and (ii) elevation of the threshold for vasopressin release (plasma osmolality 320 mmol/kg) but normal slope of the plasma vasopressin-plasma osmolality curve. Baroregulated vasopressin release was also grossly subnormal. Other hypothalamo-pituitary investigations showed deficiencies of releasing hormones for gonadotrophins and growth hormone, but prolactin response to combined hypoglycaemia and TRH was blunted She demonstrated other anomalies including hyperlipoproteinaemia and defective lymph drainage of the legs. Skull X-rays, together with computerized tomography and nuclear magnetic resonance scans of the hypothalamo-pituitary region and the rest of the brain were normal. We believe that this is the first case of essential hypernatraemia documented with direct evidence of resetting of the osmostat.
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PMID:A case of 'essential' hypernatraemia due to resetting of the osmostat. 398 72

The anteroventral third ventricle (AV3V) region plays an important role in fluid and electrolyte balance and cardiovascular control in the rat; however, experiments in other species have raised questions about the universality of findings in the rat. The effects of discrete lesions placed within the AV3V area on hydromineral balance, the pressor response to angiotensin II given intravenously, and the initiation of a renin-dependent model of hypertension were examined in the dog. A transpharyngeal approach to the optic chiasm enabled us to destroy only the anterior aspects of the AV3V region (aAV3V group) or to include the entire nucleus medianus (NM) as well (aAV3V + NM group). Lesions of the aAV3V caused polydipsia and transient hypernatremia and hyperosmolality. In contrast, adipsia and a sustained increase in plasma sodium levels and osmolality were observed in dogs with lesions of the aAV3V plus the entire NM. Neither lesion altered baseline arterial pressure, heart rate, plasma levels of catecholamines and vasopressin, or total plasma protein levels. Only in aAV3V + NM lesioned dogs was there a tendency for plasma angiotensin II immunoreactivity to be elevated above control values at 2 and 4 days after operation. Neither lesion attenuated the pressor response to intravenous angiotension II or the initiation of renal hypertension induced by aortic coarctation. As observed in other species, structures within the AV3V region participate in hydromineral balance in the dog; however, in the dog portions of the NM dorsal to the AV3V region are essential for the mediation of drinking behavior.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The anteroventral third ventricle region. Participation in the regulation of blood pressure in conscious dogs. 399 35

Electrolyte-induced myelinolysis was produced in rats to evaluate electrophysiological derangement in the brainstem. Auditory brainstem responses (ABRs) were used to assess the brainstem function. Rats treated with hypertonic saline for 2 days had normal interpeak latencies in ABRs. Rats treated with vasopressin-induced hyponatremia alone and those with hypertonic saline after 3 days of hyponatremia had significantly prolonged interpeak latencies between waves II-III and III-IV in ABRs. These prolongations indicate electrophysiological derangement of the upper pons and mesencephalon in hyponatremic rats as well as in rats with hyponatremia followed by hypernatremic myelinolysis. In view of these data, hyponatremia may be a prerequisite for electrolyte-induced myelinolysis and electrolyte derangements such as hyponatremia, and rapidly correcting hypernatremia may be the cause of electrolyte-induced myelinolysis in rats.
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PMID:Changes of auditory brainstem responses in electrolyte-induced myelinolysis in rats. Role of hyponatremia and hypernatremia. 400 6


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