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)

The renal reabsorption of water independent of solute is the result of the coordinated function of the collecting duct and the ascending limb of the loop of Henle. The unique juxtaposition of the ascending and descending portions of the loop of Henle and of the vasa recta permits the function of a counter-current multiplier system in which water is removed from the tubular lumen and reabsorbed into the circulation. The driving force for reabsorption is the osmotic gradient in the renal medulla which is dependent, in part, on chloride (followed by sodium) pumping from the thick ascending loop of Henle. Urea trapping is also thought to play an important role in the generation of a hypertonic medullary interstitium. Arginine vasopressin (AVP) acts by binding to receptors on the cell membrane and activating adenylate cyclase. This, inturn, results in the intracellular accumulation of cyclic adenosine monophosphate (AMP) which in some fashion abruptly increases the water permeability of the luminal membrane of cells in the collecting duct. As a consequence, water flows along an osmotic gradient out of the tubular lumen into the medullary interstitium. Diabetes insipidus is the clinical condition associated with either a deficiency of or a resistance to AVP. Central diabetes insipidus is due to diminished release of AVP following damage to either the neurosecretory nuclei or the pituitary stalk. Possible causes include idiopathic, familial, trauma, tumor, infection or vascular lesions. Patients present with polyuria, usually beginning over a period of a few days. The diagnosis is made by showing that urinary concentration is impaired after water restriction but that there is a good response to exogenous vasopressin therapy. Nephrogenic diabetes insipidus can be identified by a patient's lack of response to AVP. Nephrogenic diabetes insipidus is caused by a familial defect, although milder forms can be acquired as a result of various forms of renal disease. Central diabetes insipidus is eminently responsive to replacement therapy, particularly with dDAVP, a long lasting analogue of AVP. Nephrogenic diabetes insipidus is best treated with a combination of thiazide diuretics as well as a diet low in sodium and protein.
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PMID:The clinical physiology of water metabolism. Part II: Renal mechanisms for urinary concentration; diabetes insipidus. 54 67

A patient with a malignant mesothelioma developed the syndrome of inappropriate secretion of antidiuretic hormone. The electrolyte abnormalities were corrected by treatment with demethylchlortetracycline. Arginine vasopressin concentrations were increased in serum and urine. It is suggested that the syndrome might have been mediated by secretion of antidiuretic hormone from the posterior pituitary, because arginine vasopressin was not detected in the patient's tumor using a sensitive radioimmunoassay.
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PMID:Mesothelioma associated with the syndrome of inappropriate secretion of antidiuretic hormone. 64 25

Described is a patient who presented with hypernatremia in the absence of dehydration. Further investigation revealed a tumor in the hypothalamic area, and evidence of anterior pituitary hypofunction. Water loading did not correct hypernatremia, and the results of the water-loading test suggested that hypernatremia had resulted from an elevated "osmotic set point" for the release of antidiuretic hormone, ie, "essential hypernatremia."
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PMID:Essential hypernatremia. 68 42

A patient with an enlarged, asymmetric sella turcica and visual field defects suggestive of a pituitary or parasellar tumor underwent extensive roentgenographic and pituitary function studies. No abnormalities in pituitary luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, ACTH, prolactin or vasopressin secretion were detected. Growth hormone secretion was provoked by arginine infusion but not by hypoglycemia. Pneumoencephalography revealed air in the sella turcica, and no evidence of tumor. Thus, an enlarged sella turcica in a patient with visual field defects but normal pituitary function may suggest the presence of an "empty sella syndrome."
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PMID:Primary empty sella syndrome with visual field defects. 93 63

Dissatisfaction with the high morbidity and mortality of traditional methods of handling massive gastrointestinal hemorrhage has led to the exploration of means other than surgical to attain hemostasis. Some, such as selective arterial infusion of surgical Pituitrin, have quickly won general acceptance in hospitals where facilities and interested personnel are available. Others, such as alkalinization, have become popular because of their inherent simplicity. Systemic hypothermia, requiring intensive patient care, has not been without considerable risk of significant complications. Iced saline lavage has never been subjected to critical evaluation. It is possible that the emptying of the stomach through mechanical destruction of the intragastric clot by repeated irrigations, reducing the antral stimulation by relief of distension, may be as important as the temperature of the solution in the stomach. Gastric irrigations with norepinephrine solutions have awaited the results of physiologic studies showing that the cardiovascular and renal effects of injected levarterenol are avoided, and that permanent damage to the gastrointestinal mucosa does not result. Trials have been confined largely to very poor-risk patients, and the hemostasis that has resulted has not been explainable, in all cases, on the basis of the physiologic activity of the agent (e.g., control of bleeding from tumor vessels). Evacuation of gastric content prior to introduction of the norepinephrine solution seems important. Lower gastrointestinal bleeding from benign disease has also responded to advances in applied pharmacology, with intra-arterial infusion of surgical Pituitrin again coming into progressively wider use. Intraperitoneal instillation of norepinephrine has also proved useful, even in patients who have adhesions from prior surgery or inflammatory disease, but closer monitoring of blood pressure and urine output are necessary because some of this solution is absorbed by the parietal peritoneum and not deactivated by the liver before entering the systemic circulation. Taken together, selective arterial infusion of vasopressin and topical application of norepinephrine can be considered complementary rather than competitive therapies. Because of the more extensive experience with selective angiographic infusion, it should be the first choice in institutions where it is readily available. For patients in whom arterial puncture is inadvisable, and where angiography is not readily available, topically applied norepinephrine becomes the treatment of preference. We have demonstrated effectiveness of intraperitoneal norepinephrine in a patient in whom selective arterial infusion of surgical Pituitrin had failed. And the reverse would probably also hold true on occasion. Pharmacologic techniques represent a therapeutic advance, reducing the frequency with which surgical intervention becomes mandatory. But they are not a substitute for surgery...
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PMID:Massive gastrointestinal hemorrhage. 108 29

A patient with Ewing's sarcoma presented with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) (1). Plasma values for vasopressin were found to be over four times the normal values expected for the plasma osmolality. At postmortem examination, the arginine vasopressin concentration in the tumor tissue was ten times that of the plasma. These data suggest that Ewing's sarcoma may cause SIADH.
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PMID:Ewing's sarcoma as a cause of the syndrome of inappropriate secretion of antidiuretic hormone. 115 51

This is a report of the second known case of a primary malignant granular-cell tumor of the cerebral hemispherical white matter. Two cell types may be distinguished apparently representing different developmental stages of otherwise identical tumor cells. Quantitative histochemical and biochemical studies have shown that tumor cells were containing markedly elevated levels of DNA and RNA. Only few ribosomes and polysomes could be detected, however, by electron microscopy. While cytophotometry disclosed only slightly elevated cytoplasmic proteins, there was a distinct increase in total protein concentration of tumor tissue per unit weight, as measured by conventional techniques. It is suggested that this increase is mainly attributable to structural proteins of cellular and subcellular elements of multiplicating malignant cells. A ratio of RNA to DNA in excess of 1 was found for white matter derived from the central tumor, while the ratios of control tissue were lowered to values far below one due to postmortem changes greatly reducing tissue concentrations of RNA. No detailed characterization of RNA was attempted. The nuclear DNA content of tumor cells reached values equivalent to chromosomal hexadekaploidy. This was in sharp contrast to control data from an Abrikossoff tumor of the oral cavity and from a neurohypophyseal tumorette ("choristoma"), respectively, displaying diploidy only associated with a much lesser increase of cytoplasmic RNA and proteins. Qualitative lipid studies were consistent with a marked active demyelination of the tumor centre as indicated by a severe reduction of cerebrosides and sulfatides and the presence of cholesterol esters. In addition there was a striking loss of phosphatidylethanolamine and a lesser one of sphingomyelin of white matter of both the tumor-stricken and the contralateral unaffected hemispherical regions, possibly suggesting a generally disturbed metabolism of myelin. It is not clear whether these general changes were resulting from the presence of the unilateral tumor or from precocious cerebral involution.
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PMID:[Malignant granular-cell tumor of the cerebral white matter: morphological, cytophotometrical and neurochemical studies (author's transl)]. 116 67

In addition to progressive endocrine dysfunction and progressive visual loss, pituitary neoplasms may annouce their presence by the more catastrophic alternative of spontaneous tumor infarction. In two patients reported, illness due to the spontaneous infraction of pituitary tumors was heralded by sudden onset of focal headache associated with diplopia. Stupor, confusion, and evidence of increased intracranial pressure occurred without subarachnoid hemorrhage or massive extrasellar extension of tumor. One patient developed inappropriate antidiuretic hormone secretion with spontaneous infarction in a large but clinically silent chromophobe adenoma. In both patients, skull x-rays suggested a long-standing intrasella mass. Both underwent prompt treatment with endocrinologic replacement therapy and subsequent successful transsphenoidal removal of voluminous, infarcted, pituitary masses.
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PMID:Spontaneous infarction in pituitary tumors: neurologic and therapeutic aspects. 116 78

The syndrome of inappropriate secretion of antidiuretic hormone was recognized in a sixty-year-old man with a poorly differentiated metastatic adenocarcinoma of the prostate gland. Elevated levels of antidiuretic hormone were found in the patient's serum and in the prostatic tumor but not in the cerebrospinal fluid. The patient's clinical course is detailed, and the pathophysiology of this syndrome is discussed.
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PMID:Prostatic carcinoma producing syndrome of inappropriate secretion of antidiuretic hormone. 117 73

Because small cell anaplastic carcinoma of the prostate is an uncommon tumor, it has remained a poorly defined entity. To elucidate further the clinical, pathological and immunohistochemical characteristics of this cancer the 27 patients who presented to the Mayo Clinic from 1960 to 1990 were reviewed. Of these patients 18 (67%) presented with pure small cell anaplastic carcinoma, and 9 (33%) were diagnosed with small cell anaplastic carcinoma and adenocarcinoma of the prostate. Twenty-six patients (96%) had either stage C or D disease at the time of diagnosis. Two patients presented with a paraneoplastic syndrome, including 1 man with inappropriate antidiuretic hormone secretion and 1 who suffered from thyroxine intoxication. Of 24 men with long-term followup 22 (92%) died of small cell anaplastic carcinoma of the prostate despite antiandrogen therapy and the remaining 2 are alive with active, progressive disease. The median survival time following diagnosis was 17.1 months (range 2 to 90 months). All tumors with tissue available for immunohistochemical staining reacted positive for neuron-specific enolase, indicating that small cell anaplastic carcinoma of the prostate is most likely a neuroendocrine neoplasm. No tumor stained positive for either prostatic acid phosphatase or prostate specific antigen. Pathologically, small cell anaplastic carcinoma of the prostate appears to be similar to oat cell carcinoma of the lung. This series of 27 patients emphasizes that small cell anaplastic carcinoma of the prostate is highly malignant, is frequently of advanced stage at presentation, responds poorly to antiandrogen therapy and has a poor prognosis.
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PMID:Small cell anaplastic carcinoma of the prostate: a clinical, pathological and immunohistological study of 27 patients. 131 95


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