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)

1. Healthy subjects, given a long-acting preparation of vasopressin intramuscularly, excreted a significantly less concentrated urine than when subjected to fluid deprivation for 28 h. 2. When fludrocortisone, a potent mineralocorticoid, was given in addition to vasopressin the urine was not significantly less concentrated than after fluid deprivation. 3. Oral urea-loading also enhanced the urine-concentrating power of vasopressin but its effect was less marked than that of fludrocortisone. Oral urea did not increase further the urine concentration achieved by combined fludrocortisone and vasopressin. 4. Renal concentrating power was assessed in fourteen patients with renal disease and impaired concentrating ability. Fludrocortisone significantly enhanced the urine concentration achieved by vasopressin alone and the resultant urine was not significantly less concentrated than that achieved by fluid deprivation. 5. The action of fludrocortisone in enhancing the urine-concentrating effect of vasopressin is similar to that of aldosterone and is probably due to the increased sequestration of solute in the renal medulla, caused by increased reabsorption of sodium chloride in the ascending limb of the loop of Henle. 6. In the clinical assessment of renal concentrating power, the combined use of fludrocortisone and vasopressin has potential advantages over established methods.
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PMID:Assessment of urine-concentrating ability in man: effect of fludrocortisone and urea in enhancing response to vasopressin. 112 20

To examine the influence of prostaglandins (PGs) and sodium-volume status on the urinary excretion and action of arginine-vasopressin (AVP), we studied the response to a hypertonic saline infusion (2.5% NaCl, 0.06 ml/kg/min for 3 h) in 8 healthy males under three different conditions: 1) on an ad libitum salt diet (C), 2) after 4-day treatment with indomethacin (IDM) 150 mg/d, 3) after 4-day treatment with fluorohydrocortisone (9 alpha FF) 0.6 mg/d. The rise of urine osmolality and the decrease of free water clearance were identical in all three studies. Basal urinary PGE2, PGF2 alpha and AVP were decreased during IDM and unchanged during 9 alpha FF, compared to C. The increment of urinary AVP was similar during C and IDM but significantly greater with 9 alpha FF (P less than 0.02) although urinary PGs were higher at the end of the infusion. In conclusion, despite markedly different hormonal patterns and sodium status in the three protocols, the antidiuretic response to an osmolar load is preserved suggesting an adaptive mechanism maintaining a constant balance between AVP and PGs.
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PMID:Influence of a prostaglandin inhibitor and a mineralocorticoid on the antidiuretic and hormonal response to an osmolar load. 657 49

We tested the hypothesis that the fludrocortisone in doses sufficient to elevate blood pressure (BP) in normal subjects would increase platelet cytosolic calcium. Eight normal volunteers were given 0.8 mg fludrocortisone daily for 7 days (short protocol). Eight other normal volunteers ingested the drug for 6 weeks (long protocol). In the short protocol, fludrocortisone increased platelet cytosolic calcium and body weight by day 3, while BP was increased by day 7. In the long protocol, platelet cytosolic calcium was increased after 1 week, returned to basal values by 3 weeks and remained at that level for the rest of the study. Stimulation of the subjects' platelets ex vivo with thrombin and vasopressin led to a significant increase in intracellular free calcium concentration; however, fludrocortisone treatment did not alter the calcium response to either agonist. Fludrocortisone decreased serum potassium, plasma renin activity, plasma noradrenaline concentration and serum ionised calcium. These changes, as well as the BP increase, reverted to basal values when the drug was discontinued. We next incubated human platelets with fludrocortisone (1.4 nmol/l) and found a significant increase in cytosolic calcium by 30 min. The data suggest that a blood pressure-raising dose of mineralocorticoid leads to a transient (days to weeks) increase in platelet cytosolic calcium. Platelet cytosolic calcium and blood pressure are dissociated in that cytosolic calcium increases before the BP increase and later decreases to lower values, while the BP increase is sustained. Mineralocorticoid also has a direct effect on platelet cytosolic calcium in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of exogenous mineralocorticoid on platelet cytosolic calcium in normal humans. 759 7

Acute hyponatremia, following neurosurgery, results from inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting (CSW). CSW is due to abnormally high atrial or brain natriuretic peptides (ANP, BNP), which block all stimulators of zona glomerulosa steroidogenesis, resulting in mineralocorticoid deficiency. A 3 year-old girl presented CSW at day 4, after resection of craniopharyngioma and hypophysectomy. Hyponatremia, hyperkalemia and high natriuresis occurred on day 8, with low renin and aldosterone and elevated BNP 120.3 ng/ml (undetectable before surgery). Fludrocortisone 100 microg/day controlled natriuresis and restored electrolytes within 24 hours. A 5 year-old boy presented CSW at day 6 after partial resection of optic glioma. Fludocortisone 100 microg/day restored electrolytes within 8 hours. ANP was elevated, 60.6 ng/l, aldosterone and renin were low. Fludrocortisone supplementation should be considered in CSW, as excessive natriuresis is controlled, and electrolytes are easily restored, avoiding life-threatening complications of this complex disorder.
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PMID:Mineralocorticoid deficiency in post-operative cerebral salt wasting. 1805 34

Hyponatremia is the most frequent electrolyte disorder in critically ill neurological patients. The major differential diagnoses in this situation are the syndrome of inappropriate antidiuretic hormone secretion, marked by inappropriate retention of free water, and cerebral salt wasting, characterized by excessive urinary loss of sodium and resulting in polyuria and extracellular volume contraction. Cerebral salt wasting is a syndrome of hyponatremia due to increased urine output and excessive natriuresis described in patients with central nervous system disease. Although cerebral salt wasting has been well described in neurosurgical patients, data regarding pediatric patients is sparse. We present a 34-month-old boy with lissencephaly who developed cerebral salt wasting after brain biopsy. The patient was treated with hypertonic saline and multiple antiepileptic drugs. Fludrocortisone supplementation effectively treated cerebral salt wasting.
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PMID:The treatment of cerebral salt wasting with fludrocortisone in a child with lissencephaly. 2006 33

In patients with central nervous system disease, life-threatening hyponatremia can result from either the syndrome of inappropriate secretion of antidiuretic hormone or cerebral salt wasting. Clinical manifestations of the two conditions may be similar, but their pathogeneses and management protocols are different. Cerebral salt wasting syndrome is a disorder in which excessive natriuresis and hyponatremia occurs in patients with intracranial diseases. We report a 6-month-old girl with CSWS associated with tuberculous meningoencephalitis. She was diagnosed as having CSWS on the basis of hypovolemia, polyuria, natriuresis, and the relatively high level of fractional excretion of uric acid. Aggressive replacement of urine salt and water losses using 0.9% or 3% sodium chloride was done. Fludrocortisone was started at 0.1 mg twice daily on the seventh day of admission and was continued for 17 days.
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PMID:Cerebral salt wasting following tuberculous meningoencephalitis in an infant. 2256 34

Cerebral salt wasting is characterized by inappropriate natriuresis and volume contraction with associated cerebral pathology. It is distinct from the syndrome of inappropriate antidiuretic hormone secretion, which is characterized by inappropriate retention of free water. We report a patient with a porencephalic cyst who developed cerebral salt wasting. His initial treatment was supplementation of water and salt, which did not improve natriuresis or volume contraction. Fludrocortisone administration effectively managed the cerebral salt wasting.
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PMID:Cerebral salt wasting treated with fludrocortisone in a 17-year-old boy. 2266 58

Cerebral salt wasting (CSW) syndrome is an important cause of hyponatremia in head injuries apart from syndrome of inappropriate antidiuretic hormone (SIADH). Proper diagnosis and differentiation between these two entities are necessary for management as the treatment is quite opposite in both conditions. Fludrocortisone can help in managing CSW where alone saline infusion does not work. We report a 17-month-old female child with head injury managed successfully with saline infusion and fludrocortisone.
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PMID:Cerebral Salt Wasting Syndrome following Head Injury in a Child Managed Successfully with Fludrocortisone. 2721 68