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)

Two patients with the syndrome of inappropriate secretion of antidiuretic hormone were studied in a metabolic ward during treatment with 1.2 g demeclocycline daily. In both patients, demeclocycline treatment led to increased renal water excretion with consequent correction of hyponatremia and hypo-osmolality. Three episodes of reversible deterioration in glomerular filtration rate developed in these patients. Each episode was accompanied by clinical evidence of extracellular fluid volume contraction, and on each occasion there was an inappropriate natriuresis with daily urinary sodium excretion remaining above 50 mEq. Although demeclocycline effectively reverses the electrolyte abnormalities of this syndrome, the potentially dangerous side effects that may develop exclude the routine usage of the drug.
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PMID:Renal function during treatment of inappropriate secretion of antidiuretic hormone with demeclocycline. 10 Apr 73

The object was to study fluid shifts in man during the 1st h of immersion diuresis. Control experiments were done on subjects lying down in air for 4 h with and without vasopressin. During immersion up to the neck, seven of nine subjects had significant diuresis and natriuresis. In the first 20 min of sitting in 33 degress C water, a hemodilution of 2% of blood volume was observed. As diuresis progressed, hemoconcentration began. When vasopressin was given just before immersion to prevent the diuresis, the hemodilution observed was greater and lasted longer. Thus the hematocrit fell by 1.7 U, plasma osmolality by 6.0 mosmol/kg, plasma proteins by 0.33 g/100 ml, and plasma sodium by 5.0 meq/l. We conclude that a hemodilution of about 4% of blood volume occurs during the early plasma of immersion and the degree of hyposmolality observed suggests that the fluid shifted was more hyposmotic than the interstitial fluid alone, possibly because some intracellular water may have shifted into the bloodstream during immersion.
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PMID:Fluid shifts during initial phase of immersion diuresis in man. 45 49

Transient generalized oedema was observed in a patient upon exposure to a hot climate. Oedema disappeared in 5 days. Clinical study during oedema revealed decreased urine volume, high urine osmolality, high urine sodium concentration, increased blood volume, hyponatraemia and hypo-osmolality. The total solute excretion was unchanged. The endogenous creatinine and para-aminohippurate clearances were normal. The findings were suggestive of increased antidiuretic hormone activity, and heat might be responsible.
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PMID:Heat oedema: a clinical study. 53 61

The influence of the prevailing PaCO2 on the water-retaining effects of sustained elevations in ADH was assessed by administering vasopressin (5 U in oil, twice daily) and a fixed water intake to dogs with eucapnia (n, 7), chronic hypercapnia (n, 6), and chronic hypocapnia (n, 8). Although water excretion initially fell to a similar extent in all three groups, cumulative water retention by day 4 of vasopressin administration was 77 mg/kg in the hypocapnic group, 46 ml/kg in the eucapnic group, and only 14 ml/kg in the hypercapnic group. These differences were reflected in a marked disparity in the degree of hyposmolality of body fluids, plasma osmolality falling by day 4 to an average value of 223, 237, and 268 mosmol/kg in the hypocapnic, eucapnic, and hypercapnic animals, respectively. In a separate group of dogs, water deprivation and water loading studies revealed that sustained hypercapnia does not affect the maximal concentrating or diluting ability of the kidney. We conclude, therefore, that the striking influence of the prevailing PaCO2 on the water-retaining effects of administered vasopressin cannot be ascribed to an altered responsiveness of the nephron per se, but that this influence reflects an alteration in the ease with which the kidney can escape from the antidiuretic effects of this substance.
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PMID:Influence of steady-state PaCO2 on escape from ADH-induced water retention in the dog. 64 65

SIADH consists of hyponatremia and hyposmolality, continued urinary loss of sodium, excretion of an inappropriately concentrated urine, and absence of dehydration, usually in the presence of normal renal and adrenal function. The retention of excess water caused by the inappropriate secretion of antidiuretic hormone is central to the development of the syndrome. In pediatrics, SIADH is most commonly seen in patients with meningitis or postoperatively. Fluid restriction is vital in such patients to prevent the development of symptomatic SIADH. Fluid restriction alone will also result in the correction of serum electrolyte composition in patients with SIADH. Hypertonic saline should be used only in severely symptomatic patients.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion (SIADH). 79 77

The syndrome of inappropriate secretion of arginine vasopressin (AVP) known as the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is associated with a variety of malignant and nonmalignant diseases. Only 17 cases of SIADH have been reported in the literature in association with cancer isolated to the head and neck. A retrospective review of 1,436 patients with head and neck malignancy excluding skin cancer through The University of Iowa Tumor Registry revealed 60 patients with the diagnosis of either SIADH or hyposmolality. A chart review for each of these patients was then done to establish the diagnosis of SIADH through relevant laboratory values and by excluding other causes of hyposmolality and hyponatremia. In 43 of these patients (3%), SIADH was found to be associated only with the cancer of the head and neck. We conclude that the incidence of SIADH in patients with cancer of the head and neck is much higher than previously recognized. As elevated serum AVP levels may not be clinically apparent unless associated with excessive water ingestation, it is possible that an even higher percentage of patients may have increased serum AVP levels.
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PMID:Syndrome of inappropriate secretion of arginine vasopressin in patients with cancer of the head and neck. 133 68

Since it was first recognized 35 years ago, the syndrome of inappropriate antidiuretic hormone (SIADH) secretion has become the most commonly recognized cause of hyponatremia among hospitalized patients. The syndrome is caused by excessive intake of fluids when urinary dilution is impaired by physiologically inappropriate secretion or administration of vasopressin or other antidiuretic hormones. Inappropriate secretion of the hormone may be ectopic by a malignancy or ectopic and can ensure from any of three different types of osmoregulatory defects. Rarely, there is no demonstrable defect in the osmoregulation of vasopressin. The excessive fluid intake may be due to inappropriate thirst but often is iatrogenic. The syndrome occurs in association with many diseases, particularly of the lungs and brain, and can also be caused by drugs or surgery. Its principal symptoms are neurologic and due to the associated hypo-osmolality of body fluids. Diagnosis requires exclusion of certain other hormonal or hemodynamic disorders that can also increase vasopressin or impair urinary dilution. Therapy differs depending on the severity and duration of the hyponatremia but is always based on cautiously raising plasma sodium by fluid restriction, infusion of hypertonic saline, or administration of drugs that block the antidiuretic effect of vasopressin.
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PMID:Syndrome of inappropriate antidiuresis. 148 79

Hyponatremia is common following subarachnoid hemorrhage and has alternatively been attributed to either the inappropriate secretion of antidiuretic hormone or natriuresis causing intravascular volume contraction. We prospectively studied body sodium and intravascular volume regulation in 19 patients, beginning within 3 days after acute aneurysmal subarachnoid hemorrhage occurred, in order to determine the impact of hypervolemic therapy on both hyponatremia and volume contraction and to ascertain whether humoral factors account for hyponatremia. Serial measurements of plasma arginine vasopressin, atrial natriuretic factor, renin activity, aldosterone, and catecholamines were correlated with body sodium and fluid balance, change in blood volume, serum sodium concentration, and osmolality. Six patients (32%) developed hyponatremia, but only 2 had a negative sodium balance. In most patients, levels of atrial natriuretic factor were elevated, while plasma renin activity and aldosterone concentrations were generally suppressed. Plasma arginine vasopressin levels were not suppressed during hypo-osmolality and did not correlate with serum osmolality in hyponatremic patients. Only 1 patient had a decrease in blood volume, which was associated with marked rises in aldosterone and plasma renin activity, but normal serum sodium and plasma atrial natriuretic factor levels. We conclude that following subarachnoid hemorrhage: (1) Hypervolemic therapy prevents volume contraction but not hyponatremia, (2) humoral factors may favor both sodium loss and water retention, and (3) arginine vasopressin regulation is disturbed and may contribute to hyponatremia.
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PMID:Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage. 153 78

Two pregnant women developed overt polyuria (up to 11 l/day) and polydipsia during their second and third trimesters of pregnancy. In one patient hydronephrosis was present. Both patients suffered from mild gestational diabetes mellitus. Plasma sodium was 145 and 162 mmol/l. Polyuria and urinary hypo-osmolality responded well to desmopressin acetate. After delivery, polyuria and polydipsia disappeared in one patient and significantly improved in the other. Infusion of hypertonic saline one and two weeks respectively after delivery led to plasma hyper-osmolality (294 mosmol/kg and 305 mosmol/kg) without detectable stimulation of arginine vasopressin (AVP). Anterior pituitary function was normal. No stimulation of AVP occurred following insulin-induced hypoglycemia. AVP plasma disappearance after i.v. pulse injection of 1 microgram AVP as well as AVP plasma concentration after continuous infusion of 10 ng AVP/min was studied two weeks after delivery in one patient. The results suggested markedly elevated degradation of AVP compared to control subjects, probably due to an increased vasopressin activity. Eight months after delivery, hypertonic saline infusion in one patient led to a plasma-osmolality of 312 mosmol/kg without stimulation of AVP. In the second patient, AVP was not detectable (less than 0.2 pg/ml) six months after delivery when plasma osmolality was 290 mosmol/kg. Our studies demonstrate that a subclinical compensated diabetes insipidus was preexistent in both patients. Exacerbation occurred due to an increased AVP-clearance and presumably due to the hemodynamic and hormonal alterations during pregnancy, including a mild gestational diabetes mellitus.
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PMID:[Transient polyuria in pregnancy in diabetes insipidus and gestational diabetes]. 177 Sep 4

An optic chiasm glioma may cause loss of vision, endocrine disturbances, hydrocephalus and cerebral ischemia due to its proximity to the pituitary, hypothalamus, III ventricle and internal carotids. A 3-month-old infant with optic chiasm glioma developed hypopituitarism and inappropriate secretion of antidiuretic hormone with plasma hypo-osmolality. The cerebrospinal fluid (CSF) protein concentration was markedly elevated. The impairment of fluid absorption via arachnoid villi and peritoneum by the high protein content, and reversed osmotic gradient between protein-rich CSF and hypo-osmolar plasma may have contributed to both nonobstructive hydrocephalus and recurrent ascites following ventriculoperitoneal shunting. Cerebral ischemia from carotid compression may have led to cerebral atrophy.
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PMID:Optic chiasm glioma associated with inappropriate secretion of antidiuretic hormone, cerebral ischemia, nonobstructive hydrocephalus and chronic ascites following ventriculoperitoneal shunting. 179 May 31


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