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)

Hyponatremia is common following aneurysmal subarachnoid hemorrhage and has been linked to the syndrome of inappropriate secretion of antidiuretic hormone. However, the demonstration of volume depletion and natriuresis in some patients has suggested that salt wasting is a more likely etiology. Atrial natriuretic factor appears to play a role in both central and peripheral regulation of sodium homeostasis. To investigate the behavior of circulating atrial natriuretic factor following subarachnoid hemorrhage, we studied 25 patients with intracranial aneurysms: 21 after acute subarachnoid hemorrhage and four without evidence of recent rupture. Atrial natriuretic factor was measured by radioimmunoassay of extracted plasma (normal value, 20.8 +/- 24.6, mean +/- 3 SD). Mean +/- SEM plasma atrial natriuretic factor concentration was elevated to 84 +/- 25 pg/ml on Day 1, rose to 134 +/- 29 pg/ml on Day 3, and fell to 86 +/- 17 pg/ml by Day 7 after subarachnoid hemorrhage (p less than 0.01). In two patients (9.5%) who developed hyponatremia after aneurysm rupture, plasma concentrations were no different from that in the group as a whole; concentrations in patients with no evidence of recent subarachnoid hemorrhage were not elevated. Neither fluid administration nor timing of surgery could account for the elevated concentrations. We conclude that concentrations of circulating atrial natriuretic factor are elevated after subarachnoid hemorrhage but do not solely account for the accompanying hyponatremia.
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PMID:Plasma atrial natriuretic factor and subarachnoid hemorrhage. 297 Jul 2

Urinary concentrating defects and renal salt wasting have been described in the hyperbilirubinemic Gunn strain strain of rat. Homozygous animals demonstrate significant reductions in renal medullary urea and sodium ion concentrations. These observations are consistent with possible bilirubin associated disorders in the transepithelial transport of water and solute. To test this hypothesis, measurements of active sodium transport and passive water and urea fluxes were made in hemibladders isolated from the Dominican toad, Bufo marinus. Tissues were exposed to amphibian bicarbonate Ringer's solution containing 0.1 mM bilirubin with 0.05% bovine serum albumin (BSA) or BSA alone. Vasopressin-stimulated sodium transport, as reflected by short circuit current (SCC), was inhibited by 18 +/- 6% in the presence of bilirubin (N = 10; P less than 0.02). Cyclic AMP (p-Cl-phenylthio cAMP 10(-5) M) stimulated SCC was inhibited to a similar degree in the presence of bilirubin. The inhibition was noted only when bilirubin was in the serosal bath, and it could be abolished with BSA 0.5%. Bilirubin had no effect on the increase in SCC induced by higher concentrations of cyclic AMP (10(-4) M), aldosterone, or amphotericin B. Furthermore, bilirubin had no effect on the hydro-osmotic response to vasopressin and vasopressin-induced changes in urea permeability. These findings show that short-term exposure to bilirubin exerts a tissue-specific effect on the vasopressin-stimulated active transport of sodium but has no effect on the vasopressin-induced fluxes of water and urea.
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PMID:Effects of bilirubin on transepithelial transport of sodium, water, and urea. 298 53

Potassium output from the body is regulated by renal excretion, which takes place predominantly in the late distal and cortical collecting tubules. The accepted model for potassium secretion implies the accumulation of potassium into the cell by the activity of basolateral Na-K-ATPase and its exit through voltage-dependent conductive channels. The factors regulating renal potassium secretion are potassium intake, distal urinary flow, systemic acid-base equilibrium, aldosterone, antidiuretic hormone and, probably, epinephrine. Renal handling of potassium is best studied by the response to the acute administration of furosemide. This loop diuretic not only increases sodium and chloride excretion but also enhances potassium and hydrogen ion excretion and stimulates the renin-aldosterone axis. The term "renal tubular hyperkalaemia" refers to a tubular dysfunction where the hyperkalaemia is disproportionate to any reduction in glomerular filtration rate (GFR) and not due primarily or solely to aldosterone deficiency or to drugs impairing either mineralocorticoid action or tubular transport. The syndromes of renal tubular hyperkalaemia mainly observed in childhood are "chloride shunt" syndrome, hyporeninaemic hypoaldosteronism and primary or secondary pseudohypoaldosteronism. Differential diagnosis between these conditions is easily made if attention is paid to the level of GFR, presence of sodium wasting, activity of the renin-aldosterone axis and renal response to acute administration of furosemide.
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PMID:Renal tubular hyperkalaemia in childhood. 315 64

This prospective study is based on 256 patients with severe brain injury. Six patients (2.3%) developed the clinical picture of inappropriate secretion of antidiuretic hormone (SIADH): 3 in the first 3 days following the injury, 3 after more than a week. Their ADH plasmatic level were measured by radio-immunoassay. In the former, many factors, largely iatrogenic, can explain the increased secretion of ADH we found and which is then definitely "appropriate". It should be prevented by fluid restriction. In the latter, we found adequately low ADH levels, when the hypo-osmolarity is taken into account. Here, the aetiology seems to be a renal salt loss, eventually in relation to a natriuric factor (e.g. atrial natriuretic factor), justifying the term: "Cerebral salt wasting syndrome". With the resistance to fluid restriction, the treatment still remains a problem.
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PMID:Hyponatremia hypo-osmolarity in neurosurgical patients. "Appropriate secretion of ADH" and "cerebral salt wasting syndrome". 339 48

Hyponatraemia implies water retention in excess of sodium with or without increased loss of sodium from the body; extracellular fluid volume may be increased, normal or reduced. It has many causes which are briefly reviewed. Among these is the rare syndrome of inappropriate secretion of antidiuretic hormone (SIADH). It is suggested that SIADH is often diagnosed incorrectly because the raised ADH levels are appropriate for the volume status of the child. Precision in the diagnosis is important because whilst water restriction is necessary for the treatment of SIADH, other measures including the administration of extra fluid are often required if the raised ADH is appropriate. Hyponatraemia in the newborn may be caused by prerenal failure, renal failure or renal sodium wasting which is common in premature infants. Careful control of sodium intake as well as water intake is vital in this age group. Surgery is associated with water retention, but recent studies suggest that ADH levels are raised post-operatively because of volume depletion and that present recommendations for fluid therapy during and following surgery are inadequate. The use of electrolyte-free dextrose solutions should be abandoned and more liberal use of physiological saline or colloid is recommended.
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PMID:Hyponatraemia in premature babies and following surgery in older children. 360 58

We report a case of hyponatremia associated with volume depletion after pituitary exploration and biopsy. The presence of clinical dehydration precluded diagnosis of the syndrome of inappropriate secretion of antidiuretic hormone. The absence of a hypoadrenal state and the patient's response to volume reexpansion were consistent with a diagnosis of primary cerebral salt wasting.
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PMID:Cerebral salt wasting after pituitary exploration and biopsy: case report. 370 20

The maxillofacial trauma patient whose neurologic status undergoes a rapid and serious deterioration may have a severe hyponatremia secondary to the inappropriate secretion of antidiuretic hormone (SIADH). Other causes of hyponatremia must be ruled out, especially posttraumatic cerebral salt wasting, which necessitates a different mode of therapy. A case of SIADH is reported, and the work-up and differential diagnosis of posttraumatic hyponatremia are discussed.
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone in the maxillofacial trauma patient. 385 3

We studied the sodium balance and changes in plasma volume by an isotope dilution technique in the first week after an aneurysmal subarachnoid hemorrhage in 21 patients. In 11 of the patients, the plasma volume decreased by more than 10%. This was accompanied by a negative sodium balance and hyponatremia in 6 patients, a negative sodium balance without hyponatremia in 4 patients, and a positive sodium balance in 1 patient. Together with a decrease in plasma volume, blood urea nitrogen content increased and body weight decreased. Three patients developed hyponatremia without a decrease in plasma volume. Serum vasopressin was measured in 14 of the 21 patients. The values were elevated on admission and declined in the first week, regardless of the presence of hyponatremia. These findings indicate that natriuresis and hyponatremia in aneurysmal subarachnoid hemorrhage reflect salt wasting and not inappropriate secretion of antidiuretic hormone and that these changes should be corrected by fluid replacement rather than by fluid restriction.
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PMID:Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. 403 61

A case of the inappropriate secretion of antidiuretic hormone syndrome (SIADH) associated with uneventful repair of a cleft palate in a child with Pierre Robin syndrome is reported. Excess secretion of ADH is seen with pulmonary disease, intracranial infections, and trauma and as a side effect of numerous drugs. Symptoms may be vague but ultimately progress to seizure or coma. Diagnosis is made by confirming hyponatremia and serum hyposmolality in the presence of less than maximally dilute urine with relative sodium wasting. Treatment usually consists of reversing the underlying disorder, fluid restriction, and occasionally hypertonic saline or drug administration. Because of its association with neurological disorders, SIADH should be considered in any patient with an unexplained change in neurological symptoms.
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone associated with cleft palate: report of a case and review of the literature. 636 9

A 76-year-old white man was evaluated for a syndrome of hyponatremia, hypotension, and high urinary sodium excretion. There was evidence of inappropriate secretion of antidiuretic hormone and renal salt wasting in the presence of a normal glomerular filtration rate. He had a distal tubular acidification defect and unresponsiveness to standard doses of mineralocorticoids. The renin aldosterone axis was normal, as were thyroid and adrenal function. The patient could not dilute the urine, nor excrete a standard water load. Renal concentrating ability was normal, but there was no additional response to exogenous vasopressin. With modest salt restitution, the patient continued to lose large quantities of sodium in the urine, resulting in severe postural hypotension. Renal biopsy showed normal glomeruli with distinct degeneration of the distal tubules. There was no evidence of an acute inflammatory interstitial nephritis. The patient did not respond to therapeutic doses of mineralocorticoid (fludrocortisone), but treatment with water restriction, increased salt intake, and large doses of mineralocorticoids resulted in a normal serum sodium level and blood pressure. This case falls in the category of "cerebral salt wasting" syndrome. The cause was a combination of idiopathic secretion of antidiuretic hormone and distal tubular degeneration resulting in pseudohypoaldosteronism.
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PMID:Hyponatremia due to cerebral salt-wasting syndrome. Combined cerebral and distal tubular lesion. 648 51


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