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)

After unilateral release of bilateral ureteral obstruction (BUO), there is a significant increase in renal vasoconstriction that accounts for the marked decrease in glomerular filtration rate and effective renal plasma flow seen in this setting. We examined the potential role of antidiuretic hormone (ADH), a vasoconstrictor of the renal circulation, on renal hemodynamics in female Sprague-Dawley rats with BUO of 24-hr duration. Rats with BUO had significantly higher plasma values of ADH 65.1 +/- 12.2 vs. 12.1 +/- 4.1 pg/ml), sodium (145.4 +/- 0.91 vs 138.6 +/- 1.06 mEq/liter), and osmolality (375.6 +/- 2.0 vs 310.1 +/- 3.6 mOsm/kg) than sham-operated rats. Rats with BUO pretreated with enalapril, an angiotensin-converting enzyme inhibitor, before obstruction had somewhat higher, but not significantly different, plasma values for ADH (84.6 +/- 20.8 pg/ml) than rats with BUO not given enalapril. Rats with unilateral ureteral obstruction of 24-hr duration had plasma levels of ADH (8.2 +/- 1.3) not different from those in sham-operated rats. Rats with BUO pretreated with a specific antagonist of the V1-type receptor for ADH had significantly greater values for the glomerular filtration rate (2.31 +/- 0.24 vs 1.44 +/- 0.08 ml/min/kg body wt) and the effective renal plasma flow (8.95 +/- 0.71 vs 3.81 +/- 0.44 ml/min/kg body wt) and significantly lower values for mean arterial pressure (140.3 +/- 2.0 vs 159.1 +/- 5.5 mm Hg) than did BUO rats not given the antagonist. The results indicate that high levels of ADH play an important role in the decrease in the glomerular filtration rate and effective renal plasma flow observed in rats with BUO of 24 hr. The significant increase in ADH levels after BUO of 24-hr duration may be due to an increase in osmotic stimulation as a consequence of hypernatremia. Activation of the renin-angiotensin axis, known to occur after BUO or unilateral ureteral obstruction of 24-hr duration, does not appear to have a role in the increased circulating levels of ADH.
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PMID:Role of vasopressin in rats with bilateral ureteral obstruction. 202 Jun 70

A rare case of an abscess in the cavum septi pellucidi (CSP) is described and previously reported cases are reviewed. A 60-year-old male was admitted to the hospital because a diagnosis of cerebellar hemisphere infarction was made on CT scan. Seven years earlier, the patient had undergone a craniotomy for aneurysm clipping, and a ventriculo-peritoneal shunt was installed for normal pressure hydrocephalus 14 days after the aneurysmal rupture. On his second hospitalization CT scan also demonstrated CSP but this was not associated with ventriculomegaly. He was placed on a rehabilitation regimen and his hospital course was uneventful. Two months later, however, he developed hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone. After analysis of CSF obtained from the shunting device, a diagnosis of meningitis was made and CSF culture revealed E. coli infection. A part of the peritoneal tubing was torn and missing when the tube was removed from the peritoneal cavity and converted to outer drainage. Being treated with intrathecal and intravenous antibiotics administration, the meningitis subsided. However, CT scan taken twelve days after the onset of the infection showed an abscess in CSP which showed ring enhancement after contrast media. Therefore, the patient continued to receive intravenous antibiotics to counter the mass effect due to the abscess. The abscess had disappeared on follow-up CT scan obtained ten days later. The patient, however, eventually expired after iatrogenic hypernatremia associated with acute renal failure. The patient was submitted to an autopsy. The authors speculate that the abscess developed through a retrograde cisternal route after infection which had originated from bowel perforation by the peritoneal shunt tube.
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PMID:[A case report: abscess of the cavum septi pellucidi]. 202 72

The contribution of oxytocin to the maintenance of renal Na+ excretion in the Brattleboro rat has been examined in animals infused with hypotonic saline. Brattleboro rats exhibited hypernatraemia and hyperosmolality associated with greatly increased plasma concentrations of oxytocin by comparison with Long-Evans control rats. Neurohypophysectomy to remove the secretion of the remaining posterior pituitary peptide, oxytocin, led to greatly diminished rates of Na+ excretion in the Brattleboro rat. Oxytocin replacement to achieve plasma levels equivalent to those in intact Brattleboro rats produced a substantial and sustained natriuresis in the neurohypophysectomized animal. Oxytocin secretion evoked in response to saline infusion would thus appear to be effective in promoting renal Na+ excretion in the absence of vasopressin in the Brattleboro rat.
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PMID:Influence of oxytocin on sodium excretion in the anaesthetized Brattleboro rat. 203 Mar 28

Vasopressin is synthesized in the perikarya of magnocellular neurons and is transported down long axons to the storage terminals of the posterior pituitary. To maintain stable pituitary stores following vasopressin secretion, the hypothalamus must synthesize and transport an amount of new vasopressin, equivalent to the amount released. Vasopressin release and synthesis rate can be chronically upregulated or suppressed relative to basal levels, depending on the demand for vasopressin. We studied whether vasopressin transport was similarly regulated during situations of varying demand. During chronic hyponatremia, when synthesis of vasopressin was reduced to undetectable levels, transport of vasopressin was also markedly decreased, as evidenced by continued presence of vasopressin in the transport system. Upregulation of transport was demonstrated by measuring pituitary accumulation of vasopressin in rats whose pituitary stores were initially depleted by hypernatremia and in whom subsequent release was suppressed by hyponatremia. In hypernatremic rats, transport of vasopressin was increased fivefold over baseline as determined by pituitary accumulation, and this elevated rate persisted for 7 days in the absence of release. This study demonstrates that axonal transport of vasopressin is a regulated process and is linked to synthesis rate rather than release.
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PMID:Vasopressin transport regulation is coupled to the synthesis rate. 204 74

We reported an 11-year-old boy who suffered from transient hypernatremia, hypothermia, and circadian rhythm disturbances of sleep-wakefulness and body temperature from the age of 4 years, as sequelae of acute subdural hematoma. T1-weighted magnetic resonance imaging (MRI) of the brain revealed low intensity consistent with necrotic change in the whole left cerebral hemisphere, hypothalamic region, and the right-sided brain stem including tegmentum, while the pituitary structure was well preserved. Anterior pituitary function was almost normal. ADH (antidiuretic hormone) was neither stimulated by hyperosmolality nor suppressed by hyposmolality but continued to be secreted at almost constant level approximating the normal basal state. This pattern seemed to be due to complete destruction of the osmoreceptor located in the anterior hypothalamus. He exhibited a dispersed-type sleep with differentiated stages of NREM (non-rapid eye movement), although the percentage of sleep was higher at night than in the daytime. It is suggested that circadian rhythm of sleep-wakefulness and differentiation of NREM sleep stages are regulated by different neuromechanisms. Brain stem lesion on MRI may be connected with the pathogenesis of the dispersed-type sleep with special respect to amplitude reduction of sleep-waking circadian rhythm. Circadian rhythm of body temperature (BT) was irregular in amplitude, phase, and period without synchronization with sleep-wakefulness rhythm. Hypothermia was also demonstrated at the basal state, while BT increased when he suffered from respiratory infection. It is likely that hypothermia in our case is caused by the BT shift to the lower side due to malfunction of BT integrating system including preoptic area and anterior hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sodium regulation disorder, hypothermia, and circadian rhythm disturbances of the body temperature and sleep-wakefulness as sequelae of acute subdural hematoma]. 205 28

The purpose of this review is to provide an update on the use of the urine electrolyte and osmolality measurements in patients with disorders of fluid, electrolytes, and/or acid-base metabolism. It is critical to appreciate that there are no 'normal values' for these parameters, only 'expected values' relative to clinical situations. Pitfalls in the interpretation of each electrolyte in the urine are also provided. To detect a mild to moderate degree of reduction of the 'effective' intravascular volume, both urine sodium (Na) and chloride (Cl) concentrations should be measured. Pitfalls in this assessment are abnormal renal and adrenal function and the use of diuretics. Insights into the etiology of the low 'effective' intravascular volume can be deduced by comparing the urine Na, potassium (K), and Cl concentrations. The urine net charge (Cl vs. Na + K) is the most reliable way to estimate the urine ammonium concentration short of its direct measurement, an assay that is not provided by most laboratories. This measurement is important in the differential diagnosis of hyperchloremic metabolic acidosis. To examine the renal response to hypokalemia or hyperkalemia, the two components of K excretion (K secretion and urine flow rate) should be examined separately. The former is evaluated using the transtubular K, concentration gradient. The urine osmolality is used to assess antidiuretic hormone action and the osmolality of the renal medulla and to determine the etiology of polyuria and/or hypernatremia. The urine osmolality can also be used to assess the ammonium concentration, using the urine osmolal gap, and to detect unusual urine osmoles.
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PMID:Urine electrolytes and osmolality: when and how to use them. 219 Apr 69

We reported two infants with hydranencephaly and chronic hypernatremia. Their plasma sodium concentration gradually increased during the first week and remained between 150-160 mEq/L thereafter. They showed no signs of thirst. A water deprivation test demonstrated low urine osmolality and low plasma ADH concentration despite markedly elevated plasma osmolality in both cases. Urine was significantly concentrated when vasopressin was given. Thus, it was concluded that both thirst mechanism and ADH secretion were disturbed in these two cases. ADH producing cells, the thirst center and the osmoreceptor are all located in the hypothalamus. Radiographic measures showed dysplasia of the hypothalamus, providing the anatomical basis for their dysfunction.
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PMID:[Endocrinological analysis of chronic hypernatremia in two cases of hydranencephaly]. 229 50

Five children who developed diabetes insipidus as a manifestation of severe brain injury received continuous intravenous treatment with a solution containing both aqueous vasopressin and appropriate crystalloid replacement. Polyuria, hypernatraemia, and decreased urine osmolalities were safely corrected in all patients within eight to 28 hours.
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PMID:Continuous vasopressin replacement in diabetes insipidus. 240 Feb 31

Changes in blood plasma content of hormones which are observed in the different periods of hemorrhagic fever and the attendant renal syndrome are directed to the maintenance of significantly deranged water-electrolyte homeostasis. Adequate secretion of vasopressin and aldosterone in response to the changes in sodium concentration and plasma osmolality point to the absence of significant functional disorders of the corresponding glands. Pronounced hypernatremia in fatal cases is evidence of the deranged processes of osmoregulation associated primarily with kidney areactivity to vasopressin and prognostically is an unfavourable sign. The presence of pituitary necrosis in deceased subjects does not rule out the role of vasopressin deficiency in the pathogenesis of pronounced hypernatremia.
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PMID:[Pathogenesis of water-electrolyte imbalance in acute renal failure in patients with hemorrhagic fever with nephrotic syndrome]. 256 11

From 1975-1986 6 boys with congenital nephrogenic diabetes insipidus were diagnosed at the age of 3 months to 10 years. Symptoms appeared within the first few weeks of life. The diagnosis was confirmed by polyuria, low urinary osmolality (97-225 mosm/kg H20), hypernatraemia (max. 171 mmol/l) and the missing response to vasopressin. The treatment was variable; 4 boys received only hydrochlorothiazide (2-2.5 mg/kg/d) which lead to a reduction of the daily urinary volume of 26-44%. Hyperelectrolytaemia disappeared and a normal thriving could be achieved. Later an additional treatment with indomethacin (2 mg/kg/d) was necessary in 3 boys because of an increase of polyuria; there was a further reduction of the daily urinary volume of 50-60%. The combination of hydrochlorothiazide and indomethacin in the treatment of the congenital nephrogenic diabetes insipidus was well tolerated and seems to be--especially during the first few years of life--a necessary and effective treatment which allows a normal thriving and psychointellectual development.
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PMID:[Long-term course of 6 boys with congenital nephrogenic diabetes insipidus]. 260 Dec 80


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